Dros 06 Addendum

7/28/2019 Dros 06 Addendum

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SAFE TRAVEL TIPSPersonal safety demands that every attendeetake the following precautions:9 NEVER WALK ALONE ON CITY STREETS,especially after dark.9 NEVER WALK OR WAIT ALONE in desertedareas such as public or Conference facility parkinglots, hallways, and stairwells.9 ALWAYS REMOVE your badge when leaving theConference facility.9 NEVER accept a ride in an unmarked taxi orshuttle van.9 NEVER give your hotel room number to strangers.9 ALWAYS lock up money and valuables.Do not carry them with you to Conference or publicfacilities.9 Take your electronic hotel key card home with you,cut it up and discard it. It contains personalinformation much like a credit card and should behandled accordingly.


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47th Annual Drosophila Research ConferencePROGRAM ADDENDUM

Friday, March 31 Platform Presenter Changes

Cytoskeleton and Cellular Biology Lanier Grand Ballroom A-B26 - 8:45 am Fragile X mental retardation protein 1 (FMR1) is required for Drosophila cellularizationFirst author O. Papoulas replaced by J . C. Sisson.Gametogenesis and Sex Determination Lanier Grand Ballroom A-B90 6:00 pm A nuclear hormone receptor that affects spermathecae number and fertility.First author name changed to Anna K. Allen.Organogenesis Ballroom of the Americas D-F83 - 6:15 pm Rac function in epithelial tube morphogenesisFirst author Carolyn Pirraglia replaced by Monn Monn Myat.

Schedule Change/Addition2:30 pm FlyMine Demonstration has been changed to 2:00 pm (Level Three, Room 336)3:304:00 pm Additional FlyMine Demonstration (Level Three, Room 336)

Saturday, April 1 Platform Presentation CancellationPattern Formation I Ballroom of the Americas D-F106 - 10:00 am Regulation of S-phase entry in the developing eye by the bHLH transcription

factor, net. Ryan Herbert. Platform Presentation Cancellation and ReplacementTechnique and Genomics Ballroom of the Americas A-C99 - 10:15 am Cancelled: BDGP Gene Disruption Project update. Robert W. Levis.

(Now poster presentation/board 781C)

99 - 10:15 am Replaced by: The Carnegie protein trap collection: a versatile research resource.Michael Buszczak1, Shelley Paterno1, J ulia Bachman1, Dan Lighthouse1, 2, Ben Ohlstein1,Anna K. Allen*1, 2, Todd Nystul1, Tina Tootle1, Erika Matunis3, Terence Murphy1, StephanieOwen1, Nathathai Srivali1, Megan Kutzer1, Eva Decotto1, J ames Wilhelm1, Allan Spradling1.(*name changed from Anna Krueger)(Formerly poster presentation/board 781C)

Schedule Change/Addition2:30 pm FlyMine Demonstration has been changed to 2:00 pm (Level Three, Room 336)3:304:00 pm Additional FlyMine Demonstration (Level Three, Room 336)


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Poster Presenter/Co-Author ChangesPoster #278A Co-author names, Peter Gallant and Walter Schaffner, removed from abstract

499C Co-author name corrected to Zhigang J in

780B J ian J in, substitute presenter for Mark Biggin

Poster Presentations CancelledPoster # 1st Author157C Elizabeth Caygill

175C Louise OKeefe

184C J ulie Brill

222B Corinna Lehmann

250C Tuba H. Sural

285B Pado Struffi

376C Yu Chen

486B J ochen Trauner

579B Irene Miguel-Aliaga

580C Irene Miguel-Aliaga

655C Claire Hinkley

715C Bruce Bryan

756B Anne D. Plessis

828B Paymaan J afar-Nejad

Additional ExhibitorsVIEWPOINT LIFE SCIENCES, INC. Booth 2042550 Bates Street, Ste 404Montreal, QC, H3S 1A7Canadatel: (514) 343-5003fax: (514) 343-5023e-mail: [email protected]: http://www.VPLSI.com

ViewPoint LS design systems for automation of behavior analysis. We can provide you with complete solutions to fityour needs from hardware to software.

VideoTrack system measures animal locomotion and behavior.

Numeriscope is a smart digital video recorder for life sciences.

LabWatcher is an event recorder.


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Additional Exhibitors, continuedCLEVER SYS, INC. Booth 30311425 Issac Newton SquareSuite 202Reston, VA 20190tel: (703) 787-6946fax: (703) 757-7467e-mail: [email protected]: www.cleversysinc.com

Headquartered in metropolitan DC area, Clever Sys., Inc., (CSI) develops and sells products and services for labanimal behavior analysis, including rodents, Drosophila, zebra fish, primates, etc. CSIs products are built withtechnologies of next generation, utilizing information of animal full body and body parts, providing measurementsof novel behavioral paradigms and new parameters that have never been available before.

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y Late Poster Abstracts (see complete text of abstracts beginning on page 12):First Author/Presenter Poster # Abstract Title and Co-AuthorsCELL DIVISION AND GROWTH CONTROL

Tom Hartl 880CThe condensin subunit CapH2 ensures faithful separation of malemeiotic chromosomes. Tom Hartl, Sarah Sweeney, Paula Campbell,Giovanni Bosco. Dept Molec & Cellular Biol, Univ Arizona, Tucson.

Michael Anderson 881AA functional genomics screen identifies Mat89Bb as a novel cell cycleregulator. Michael Anderson, Laura Lee. Dept Cell & DevelopmentalBiol, Vanderbilt Univ, Nashville, TN.

Maxim Pilyugin 882B

A role of histone chaperon ASF1 and Tousled-like kinase in cell cycleprogression. Maxim Pilyugin1, Yuri Moshkin2, Franois Karch1.1) University of Geneva, Switzerland; 2) Erasmus University MedicalCentre, Netherlands.

Violaine Mottier 883C

Misato is required for centrosome separation in both mitosis and malemeiosis. Violaine Mottier, Fiammetta Verni, Giovanni Cenci, Maurizio Gatti,Silvia Bonaccorsi. Genetica e Biologia Moleculare, Universita di Roma Lasapienza, Roma, Italy.

Alan Wainman 884ACharacterization of ZW10 in Cytokinesis. Alan Wainman, Maria GraziaGiansanti, Michael Goldberg, Maurizio Gatti. Genetica e Biologiamoleculare, Universita di Roma La Sapienza, Roma, Italy.

Wei Li 885BMechanisms and effects of cell death in Minute-induced cell competition.Wei Li, Nicholas E. Baker. Dept. of Molecular Genetics, Albert EinsteinCollege of Medicine, Bronx, NY 10461.

Roman Sidorov 886C

The role of the gene white in increase of mosaic clone frequency inD.melanogasterand D. simulans.Roman Sidorov1, Elena Ugnivenko2, KirillKirsanov2, Elizabeth M. Khovanova2. 1) Inst Carcinogenesis, CancerResearch Center RAMS, Moscow, Moscow Region, Russian Federation; 2)Koltzov Institute of Developmental Biology RAS, Moscow, Moscow Region,Russian Federation.

Stephen T. Guest 887A

A Protein Interactin Map Guided Screen for Novel Regulators of the CellCycle. Stephen T. Guest1, Maria A. Cypher1, Russell L. Finley J r.1, 2.1) Center for Molecular Medicine and Genetics; 2) Department ofBiochemistry and Molecular Biology, Wayne State University School ofMedicine, 540 East Canfield Ave, Detroit Michigan 48201.

Zuohe Song 888B

The Regulation of the Tumor Suppressor Activity, PTEN by ThioredoxinControls Cell Number and Cell Size. Zuohe Song1,2, Negin Saghafi1, MarcBrabant1,3, Emmanuelle Meuillet1,2,3. 1) Arizona Cancer Ctr, Univ Arizona,

Tucson, AZ; 2) Nutritional Sciences Department, University of Arizona,1177 E. 4th Street, Tucson, AZ. 85721; 3) Molecular and Cellular BiologyDepartment, University of Arizona, Tucson, AZ. 85724.

CYTOSKELETON AND CELLULAR BIOLOGY

Guang-Chao Chen 889C

Regulation of autophagosome formation by paxillin during nutrient stressand development. Guang-Chao Chen1,3, Sheila Thomas2, J effreySettleman1. 1) MGH Cancer Center, Charlestown, MA; 2) Beth IsraelDeaconess Medical Center and Harvard Medical School, Boston, MA;3) Inst of Biological Chemistry, Academia Sinica, Taipei, Taiwan.

Douglas Corrigall 890ARegulation of Cell Shape During Eye Organogenesis. Douglas Corrigall,Franck Pichaud. MRC Laboratory for Molecular Cell Biology, UCL, London,United Kingdom.


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MasyasuHirano

891B

The role of Planar Cell Polarity Effector genes in the embryonic epidermis. MasyasuHirano1, J anie Coe1, Obianuju Dike1, Nan Ren2, Paul Adler2, Simon Collier1.1) Dept Biological Sci, Marshall Univ, Huntington, WV; 2) Dept. Biology, University ofVirginia.

Manish

J aiswal892C

Regulation of epithelial cell-cell adhesion during wing development in Drosophila. ManishJ aiswal, Pradip Sinha. Bio Sci & Bioengineering, Indian Institute Technology, Kanpur,India.

Ella Palmer 893AA role for the Tuberous Sclerosis Complex during photoreceptor apical membranedifferentiation. Ella Palmer, Franck Pichaud. Anatomy and Developmental Biology, UCL.MRC LMCB & CBU, Gower Street, London. WC1E 6BT, United Kingdom.

KrishanuRay

894BMotors and Morphogenesis: Role of Dynein and Dynactin in testicular fusome assemblyinDrosophila. Krishanu Ray, Anindya Ghosh-Roy, Rishita Chengede, Madhura Kulkarni.Dept. of Biological Sciences, Tata Inst. Fund. Res. (TIFR), Mumbai, Maharashtra, India.

FlorianUlrich

895CIn vivoanalysis ofDrosophilaventral furrow formation. Florian Ulrich, Eric Wieschaus.Dept Molecular Biol, Princeton Univ, Princeton, NJ .

SlobodanBeronja

896ACadherin-catenin complex regulates plasma membrane localization of the exocystcomplex component Sec6. Slobodan Beronja, Ulrich Tepass. Department of Zoology,University of Toronto, ON, Canada.

GiovannaMottola

897BEndocytic control of wing development in Drosophila m. Giovanna Mottola1,2, EricMarois1, Suzanne Eaton1, Marcos Gonzlez-Gaitn1, Marino Zerial1. 1) Max PlanckInstitute for Cell Biology and Genetics, Dresden, Germany; 2) Dipartimento di Biochimicae Biotecnologie Mediche, Universita' di Napoli Federico II, Napoli, Italy.

Neal T.Sweeney

898C

Control of Neuronal Morphogenesis and the Delta/Notch Signaling Pathway by Shrub, aNovel Coiled-Coil Protein in Drosophila. Neal T. Sweeney1, 2, J ay E. Brenman3, Yuh NungJ an2, 4, Fen-Biao Gao1, 2, 5. 1) Gladstone Institute of Neurological Disease at UCSF, SanFrancisco, CA; 2) Neuroscience Program, UCSF, San Francisco, CA; 3) Department ofCell and Developmental Biology and Neuroscience Center University of North Carolina,Chapel Hill, NC; 4) Department of Physiology and Howard Hughes Medical Institute,UCSF, San Francisco, CA; 5) Department of Neurology, UCSF, San Francisco, CA.

Sang-ChulNam

899ADomain-specific early and late function of Dpatj in Drosophila photoreceptor cells. Sang-Chul Nam, Kwang-Wook Choi. Department of Molecular and Cellular Biology, BaylorCollege of Medicine, Houston, TX 77030.

J ulie Tan 900BThe role of phosphatidylinositol 4-kinase III in development. J ulie Tan1,2, J ulie Brill1,2. 1)Developmental Biology, Hospital for Sick Children, Toronto, ON, Canada; 2) Molecularand Medical Genetics, University of Toronto, ON, Canada.

GENOME AND CHROMOSOME STRUCTUREJ ennifer A.Armstrong

901CCHD1: a chromodomain-containing chromatin remodeling factor. J ennifer A. Armstrong,Matthew S. Berger, J ennifer M. Lee, Ivy E. McDaniel, Nick L. Reeves. J oint ScienceDept, Claremont Colleges, Claremont, CA.

MeridithToth

902ADeciphering chromatin based cellular processes in development using a dominantnegative histone acetyltransferase. Meridith Toth, Xianmin Zhu, Neetu Singh, FeliceElefant. Dept Bioscience/Biotechnology, Drexel Univ, Philadelphia, PA.

Craig M.Hart 903B

A dominant negative form of the BEAF insulator proteins disrupts chromatin structure.

Craig M. Hart, Matthew Gilbert, Swarnava Roy, Yian Yee Tan. Dept Biological Sciences,Louisiana State Univ, Baton Rouge, LA.

EdwardRamos

904CIdentification and Characterization of Gypsy-like Endogenous Insulators in D.melanogaster. Edward Ramos, Kelly Baxter, Victor Corces. Dept of Biology, J ohnsHopkins University, Baltimore, MD.

KarenWeiler

905AMapping and mutagenesis of the E(var)3-9locus. Karen Weiler. Dept of Biology, WestVirginia University, Morgantown, WV.


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Simon Titen 906B

Transmission of Fragment Chromosomes Lacking An Endogenous Telomere.SimonTiten, Kent Golic. Dept Biol, Univ Utah, Salt Lake City, UT.Xiao-FengZheng

907CCharacterizing Drosophila telomeres that lack natural transposons.Xiao-FengZheng, Yikang Rong. Lab of Molecular Cell Biology, National Cancer Institute,Bethesda, MD.

Xiaolin Bi 908A

Partially redundant roles of Drosophila ATM and ATR checkpoint kinase for telomeremaintenance. Xiaolin Bi1, Deepa Srikanta1, Laura Fanti2, Sergio Pimpinelli2, YikangRong1. 1) NCI/NIH, Bethesda, MD; 2) Dipartimento di Genetica e BiologiaMolecolare,Universita di Roma"La Sapienza," Rome, Italy.

REGULATION OF GENE EXPRESSIONVincent C.Henrich

909BA mutational analysis of ecdysone receptor and Ultraspiracle interaction in aheterologous cell culture system. Vincent C. Henrich, J osh Beatty, J enna Callender.Inst. Health, Science, and Soc, University of North Carolina-Greensboro.

Qin Wei 910C

Disruption of gene function by targeted insertion and inducible RNAi demonstratenautilus is essential for embryonic myogenesis and viability and impacts founder cellpatterning. Qin Wei1, Yikang Rong2, Bruce Patterson1. 1) Laboratory of Biochemistry,NCI/NIH, Bethesda, MD; 2) Laboratory of Cellular and Molecular Biology, NCI/NIH,

Bethesda, MD.

Martha Klovstad 911A

Eif1A mutations dominantly suppress the eggshell patterning defect caused byactivation of the meiotic recombination checkpoint. Martha Klovstad1, Gail Barcelo1,Uri Abdu2, Trudi Schpbach1. 1) HHMI, Molecular Biology Dept., PrincetonUniversity, Princeton, NJ ; 2) Dept. of Life Sciences, Ben-Gurion University.

VijayalakshmiRamakrishnan

912BRegulation of Histone Acetyltransferase during Development. VijayalakshmiRamakrishnan. Drexel University, Philadelphia, PA.

Neetu Singh 913CFunctional characterization of the histone acetyltransferase Elp3 duringdevelopment. Neetu Singh, Felice Elefant. Dept Bioscience/Biotechnology, DrexelUniversity, Philadelphia, PA.

Xianmin Zhu 914AFunctional analysis of the chromatin regulator protein: TIP60.Xianmin Zhu, FeliceElefant. Dept Bioscience/Biotechnology, Drexel Univ, Philadelphia, PA.

Omar S. Akbari 915B

Functional analysis of promoter-enhancer interactions at the Drosophila bithorax

complex. Omar S. Akbari, Esther Bae, Robert Drewell. Biology, University ofNevada, Reno.

SIGNAL TRANSDUCTION

Baoxue Ge 916C

Drosophila TAB2 is required for the immune activation of JNK and NF-kappaB.Baoxue Ge1, Zi-Heng Zhuang1, Lei Sun1, Ling Kong1, J un-Hao Hu1, Ming-Can Yu1,Peter Reinach2, J in-Wu Zang1. 1) Institute of Health Sciences, Shanghai, China; 2)Department of Biological Sciences, SUNY College of Optometry, New York, NY10036.

Baoxue Ge 917A

Regulation of Drosophila p38 activation by specific MAP2 kinase and MAP3 kinasein response to different stimuli. Baoxue Ge1, Zi-Heng Zhuang1, Yuan Zhou1, Ming-Cai Yu1, Neal Silverman2. 1) Institute of Health Sciences, Shanghai, China; 2)Division of Infectious Disease, Department of Medicine, University of Massachusetts

Medical School, 364 Plantation St, Worcester MA 01605.

Ning Wang 918BRole of PP2A in visual signaling. Ning Wang, Bih-Hwa Shieh. Dept of Pharmacology,Vanderbilt University, Nashville, TN.

Dong Yan 919C

Drosophila glypican Dally-like is essential for Breathless mediated trachealdevelopment in embryos and wing discs. Dong Yan1,2, Xinhua Lin1,2. 1) Division ofDevelopmental Biology, Cincinnati Children's Hospital, Cincinnati, OH; 2) Molecularand Developmental Biology Graduate Program, University of Cincinnati, OH.


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Li Xiao 920A

The Rac1 and Rac2 C-terminal Regions Interact Differently with dPosh and Ter94.Li Xiao, Douglas Ruden. Environmental Health Sciences, University of Alabama atBirmingham.

Kiranmai

Kocherlakota921B

An investigation of the oligomerization properties of SNS during myoblast fusion.Kiranmai Kocherlakota1,2, Erika Geisbrecht1, Susan Abmayr1. 1) Stowers Institute forMedical Research, 1000 E 50th Street, Kansas City, MO 64110; 2) Cell andDevelopmental Biology Department, Huck Institute of Life Sciences, PennsylvaniaState University, PA 16802.

XiaoyanZheng

922C

The Ihog cell surface proteins bind and mediate response to the Hedgehog signal.Xiaoyan Zheng2, Shenqin Yao2, Lawrence Lum2, 4, Philip Beachy1, 2, 3. 1) HowardHughes Medical Institute; 2) Molecular Biology and Genetics, The J ohns HopkinsUniversity School of Medicine, Baltimore, MD; 3) Department of Oncology, The J ohnsHopkins University School of Medicine, Baltimore, MD; 4) Current address:Department of Cell Biology, Univeristy of Texas Southwestern Medical Center, Dallas.

Sekyung Oh 923A

Reconstitution of Hedgehog signaling from exogenously introduced pathwaycomponents. Sekyung Oh, Philip A. Beachy. Molecular Biology & Genetics, HowardHughes Medical Institute, The J ohns Hopkins University School of Medicine,Baltimore, MD.

BernhardHovemann

924B

Drosophila cysteine peptidase Tan: expression in photoreceptor cells R1-R8 lendssupport for a putative histamine neurotransmitter / carcinine cycle betweenphotoreceptor terminals and epithelial glia. Bernhard Hovemann1, Stefanie Wagner1,Christiane Heseding1, J ohn True2. 1) Dept Chemistry, Ruhr Univ, Bochum, Germany;2) Department of Ecology and Evolution, State University of New York, Stony Brook,NY 11794-5245.

PATTERN FORMATIONHyunsuk Suh 925C

Identification of a novel gene that is regulated by engrailedand functions in Drosophilaembryo segmentation. Hyunsuk Suh, J eongbin Yim. Biological Sciences, SeoulNational University, Seoul, Korea.

Byeong J . Cha 926A

Kinesin and Dynein are required for anterior-specific bicoidmRNA transport in theDrosophilaoocyte. Byeong J . Cha1, William E. Theurkauf2. 1) Dept Cell &Developmental Biol, Vanderbilt Univ Medical Ctr, Nashville, TN; 2) Program inMolecular Medicine, University of Massachusetts Medical School, Worcester.

Tariq Maqbool 927B

Differentiation and identity of the Drosophila leg muscles: roles of the FGF pathwayand homeodomain transcription factor Ladybird.Tariq Maqbool, Cedric Soler, TeresaJ agla, J ean Philippe Da Ponte, Krzysztof J agla. INSERM.384, Faculty of Medicine, 28-Place Henri Dunant, 63000-Clermont-Fd, France.

Yu-Chin Lin 928C

Characterizing the Role ofDrosophilaLanA in Ommatidial Development. Yu-ChinLin1,2, Pei-I Tsai1, Cheng-Ting Chien1. 1) Academia Sinica, Institute of MolecularBiology, Taipei, Taiwan; 2) Institute of Neuroscience, National Yang-Ming University,

Taipei, Taiwan.Andrew

Tomlinson929A

The Control of Ommatidial Death in the Peripehry of the Fly Eye. Andrew Tomlinson,Hui-Ying Lim. Dept Genetics & Development, Columbia Univ, New York, NY.NagarajanUsha 930B

Functional characterization ofCG32062, the Drosophilahomologue of human Ataxin-2

Binding Protein. Nagarajan Usha, LS Shashidhara. Centre for Cellular and MolecularBiology, Hyderabad, AP, India.GAMETOGENESIS AND SEX DETERMINATION

Yu Chen 931CCutoff, a potential exoribonuclease associated protein, is required forDrosophilaoogenesis. Yu Chen1, 2, Trudi Schpbach1, 2. 1) Howard Houghes Medical Institute;2) Department of Molecular Biology, Princeton University.


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ElizabethEldon

932AA role for the Toll-like receptor, 18-Wheeler, in ovarian follicle cell migration. ElizabethEldon, Dominic Siler, Cassandra Kleve, Marie Alpuerto. Dept Biological Sci, CaliforniaState Univ, Long Beach.

Horacio M.Frydman

933BWolbachia preferentially populate the somatic stem cell niche. Horacio M. Frydman1,2,J ennifer Li1,2, Drew Robson1,2, Eric Wieschaus1,2. 1) Howard Hughes Medical Institute;2) Dept Molecular Biol, HHMI, Princeton Univ, Princeton, NJ .

J ason Burgess 934CPhosphatidylinositol 4-kinase type II is required for spermatogenesis inDrosophila.J ason Burgess, Ho-Chun Wei, Gordon Polevoy, J ulie A. Brill. Dept Developmental Biol,Rm 13-401-M, Hospital for Sick Children, Toronto, ON, Canada, M5G 1L7.

ThomasFellner

935A

lucky luke (luke), a novel gene with a potential function in asymmetric stem celldivision. Thomas Fellner1, Allyson Spence1, Cordula Schulz2. 1) Department ofDevelopmental Biology, Stanford University School of Medicine, Stanford, CA; 2) ColdSpring Harbor Laboratories, Cold Spring Harbor, NY.

ORGANOGENESIS

Selen

Muratoglu 936B

Regulation ofDrosophilaFriend of GATA gene, u-shaped, during hematopoiesis:A direct role for Serpent and Lozenge. Selen Muratoglu1, Betsy Garratt1, KristyHyman2, Kathleen Gajewski2, Robert A. Schulz2, Nancy Fossett1. 1) Center forVascular and Inflammatory Diseases and the Department of Pathology, University ofMaryland School of Medicine, Baltimore, MD 21201; 2) Department of Biochemistryand Molecular Biology, Graduate Program in Genes & Development, The Universityof Texas M. D. Anderson Cancer Center, Houston, TX 77030.

Ingolf Reim 937C

Expression and mutual repression oftinmanand the Dorsocrossgenes establishesdiversified cardiac cell identities in the dorsal vessel. Ingolf Reim1, Stphane Zaffran2,Manfred Frasch1. 1) Mol., Cell & Dev. Biology, Mount Sinai School of Medicine, New

York, NY; 2) Dev. Biology Inst. of Marseille-Luminy, Marseille, France.

Michael Taylor 938APositive and Negative Control of Muscle Differentiation. Michael Taylor, David Liotta.Sch Biosciences, Cardiff Univ, Cardiff, United Kingdom.

NEUROGENETICS AND NEURAL DEVELOPMENT

Seungbok Lee 939B

The F-actin/Microtubule crosslinker Shot is a platform for Krasavietz-mediated

translational regulation of midline axon repulsion. Seungbok Lee1, Seongsoo Lee1,Peter Kolodziej2. 1) School of Dentistry, Seoul National Univ, Seoul, Korea; 2)Department of Cell and Developmental Biology, Vanderbilt University Medical Center,Nashville, TN.

Daiki Umetsu 940CHighly ordered assembly of retinal axons and their synaptic partners is regulated byHedgehog/Single-minded in Drosophilavisual system. Daiki Umetsu, SatoshiMurakami, Makoto Sato, Tetsuya Tabata. Dept Cell Biol, IMCB Univ of Tokyo, J apan.

Songhee Kim 941AScreening of novel genes related to neuronal apoptosis mediated by dAPP-BP1pathway in D. melanogaster. Songhee Kim, Kiyoung Kim, J oohee Lee, J ongwoo Ryu,J eongbin Yim. School of Biological Sciences, Seoul National University, Seoul, Korea.

BrianDunkelberger

942BConfocal analysis of theDrosophilamutantsmall mushroom bodies (smu)reveals anabnormal cell number and axonal pattern. Brian Dunkelberger, Christine Serway,Steven de Belle. University of Nevada, Las Vegas, 89154-4004.


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MichelleBrooks-Pigott

943C

Analysis of the role of Drosophila Phosphotyrosyl phosphatase activator (D-Ptpa) inperipheral nervous system development. Michelle Brooks-Pigott1,2,3, Eddy Van Daele4,Veerle J anssens5, Christine Van Hoof5, J ozef Goris5, Koen Norga1,2,6, PatrickCallaerts1,2,3. 1) Laboratory of Developmental Genetics, Flanders Institute ofBiotechnology (VIB); 2) Center for Human Genetics, University of Leuven, Leuven,BE; 3) University of Houston, Department of Biology and Biochemistry, Houston, Texas

(former affiliation); 4) University of Sussex, School of Biological Sciences, Brighton,UK; 5) University of Leuven, Afdeling Biochemie, Faculteit Geneeskunde, DepartementMoleculaire Celbiologie, Leuven, BE; 6) Childrens Hospital, University of Leuven,Leuven, BE.

NEURAL PHYSIOLOGY AND BEHAVIORLixian Zhong 944A

The Drosophila Mutant oblivious Is Defective In Nociception. Lixian Zhong4, W. DanielTracey1,2,3. 1) Dept. of Anesthesiology; 2) Dept. of Cell Biology; 3) Dept. of Neurobiology;4) Dept. of Pharmacology, Duke University, Durham, NC.

Quan Yuan 945B

A Sleep-promoting Role for the Drosophila Serotonin Receptor 1A. Quan Yuan1, WilliamJ oiner2, Amita Sehgal1, 2. 1) Howard Hughes Medical Institute; 2) Center for Sleep andRespiratory Neurobiology, University of Pennsylvania, School of Medicine, Philadelphia,PA.

Kyung-AnHan

946CClassical reward conditioning in D. melanogaster. Kyung-An Han, Young-Cho Kim, Hyun-Gwan Lee. Department of Biology, Pennsylvania State Univ, University Park.

Michael J .Krashes

947ADrosophila Dorsal Paired Medial neurons provide a general mechanism for prolongingmemory. Michael J . Krashes, Alex C. Keene, J essica A. Bernard, Scott Waddell.Neurobiology, Univ of Massachusetts Medical School, Worcester.

Andreas S.Thum

948BMultiple memories ofDrosophilasugar reward learning. Andreas S. Thum, MartinHeisenberg, Hiromu Tanimoto. Department of Genetics and Neurobiology, University ofWrzburg, Biozentrum am Hubland, Germany.

YanshanFang

949C

Protein Phosphatase 1 Regulates the Stability of Drosophila Circadian Clock Proteins.Yanshan Fang, Sriram Sathyanarayanan, Amita Sehgal. Howard Hughes MedicalInstitute, Department of Neuroscience, University of Pennsylvania School of Medicine,Philadelphia, PA 19104.

XiangzhongZheng

950A FOXO and insulin signaling regulate the sensitivity of circadian clock to oxidative stress.Xiangzhong Zheng, Amita Sehgal. Dept. Neurosci, 232 Stemmler Hall, Univ.Pennsylvania Med. Sch./HHMI, Philadelphia, PA 19104.

EVOLUTION AND QUANTITATIVE GENETICSMargaritaRamos

951BEvolution Through the Eyes of a Fly. Margarita Ramos, Alistair McGregor, David Stern,Peter Grant. Ecology and Evolutionary Biology, Princeton University, Princeton, NJ .

IMMUNE SYSTEM AND CELL DEATH

Alain Vincent 952C

Collier/Knot is required for PSC formation and control of blood cell homeostasis. AlainVincent1, J oanna Krezmien1, Rami Makki1, Laurence Dubois1, J ean Michel Ubeda2, MarieMeister2, Michle Crozatier1. 1) Centre de Biologie du Dveloppement, CNRS/Universit,Toulouse, France; 2) Institut de Biologie Molculaire et Cellulaire, CNRS, Strasbourg,

France.


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Lihui Wang 953A

Establishing the molecular events during pattern recognition of Gram-positivein Drosophila innate immunity. Lihui Wang1, Alexander Weber2, Sergio Filipe3,s Gay2, Petros Ligoxygakis1. 1) Genetics Unit, Department of Biochemistry,ty of Oxford, South Parks Rd OX1 3QU, Oxford UK; 2) Department ofistry University of Cambridge, 80 Tennis Court Road, CB2 1GA Cambridge UK;to de Tecnologia Qumica e Biolgica / Universidade Nova de Lisboa, Av. da

a (EAN), Apartado 127, 2781-901 Oeiras, Portugal.

J ulienColombani

954B

Dmp53 activates the Hippo pathway to promote cell death in response to DNAdamage. J ulien Colombani, Cedric Polesello, Filipe J osue, Nicolas Tapon.Apoptosis and Proliferation Control Lab, Cancer Research UK, London Institute,United Kingdom.

Katherine A.Taylor

955C

Alteration of gravitational force affects the immune response. Katherine A.Taylor1, Alexander T. Kloehn1, Patrick M. Fuller2, Kathleen M. Beckingham3,Charles A. Fuller2, Deborah A. Kimbrell1. 1) Molecular & Cellular Biology,University of California, Davis, CA; 2) Neurobiology, Physiology & Behavior,University of California, Davis; 3) Dept. Biochemistry and Cell Biology, RiceUniversity, Houston, TX.

TECHNIQUES AND GENOMICS

AlbertCespedes

956A

An efficient genetic screen in Drosophila to identify nuclear-encoded genes withmitochondrial function. Albert Cespedes1,2, T. S. Vivian Liao1,2, Gerald B. Call1,2,Preeta Guptan1, J amie Marshall1, Edward Owusu-Ansah1, Sudip Mandal1, Q.Angela Fang1, Kevin Yackle1, Gelsey L. Goodstein1, William Kim1, UtpalBanerjee1. 1) Mol., Cell and Dev. Biology, UCLA, Los Angeles, CA; 2) Theseauthors contributed equally to this work.

StephenRichards

957B

Insect Sequencing at the Baylor College of Medicine Human GenomeSequencing Center. Stephen Richards1, Yue Liu1, Kim C. Worley1, EricaSodergren1, Steven E. Scherer1, Catherine M. Rives1, Susan Brown2, RichardBeeman3, J ohn H. Warren4, Donna M. Muzny1, George Weinstock1, Richard A.Gibbs1. 1) Human Genome Sequencing Center, Baylor College of Medicine,Houston TX; 2) Division of Biology, Kansas State University, Manhattan, KA; 3)USDA, Biological Research Unit, 1515 College Ave, Manhattan, KA; 4)Department of Biology, University of Rochester, NY.

Yung-HengChang

958C

Use Drosophila as A Model System to Identify the Function of Human Genes.Yung-Heng Chang1,2, Y. Henry Sun2. 1) Graduate Institute of Life Sciences,National Defense Medical Center, Taipei 114, Taiwan, Republic of China; 2)Institute of Molecular Biology, Academia Sinica, Taipei 115, Taiwan, Republic ofChina.

DROSOPHILA MODELS OF HUMAN DISEASES

Wing ManChan

959A

An inducible Drosophila cell model to study polyglutamine disease. Wing ManChan1,2, Pang Chui Shaw2, Edwin HY Chan1,2. 1) Laboratory ofDrosophilaResearch, The Chinese University of Hong Kong, HKSAR, China; 2) MolecularBiotechnology Program, Department of Biochemistry, The Chinese University ofHong Kong, HKSAR, China.


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LasbleizChristelle

960B

A New Drosophila model for SCA7 polyglutamine disease demonstrates reversibleity and allows quantitative screening for phenotypic modifiers. Lasbleiz Christelle1,Vronique1, Latouche Morwena2, Brice Alexis2, Stevanin Govanni2, Tricoire Herv1. 1)ques Monod, Paris, France; 2) Institut des Neurosciences, Paris, France.

Allyson

Spence961C

D. melanogasteras a model of mammalian hematopoiesis: characterization of thespaghetti mutant. Allyson Spence, Thomas Fellner, Margaret Fuller. Departmentof Developmental Biology, Stanford University School of Medicine, Stanford.

Kyu-Sun Lee 962A

Over-expression of J NK signaling rescues electromagnetic stress induced lethality inDrosophila. Kyu-Sun Lee1, J ang-Yul Kwak2, Dong-Seok Lee3, Kweon Yu1. 1)Development & Differentitation, KRIBB, Daejeon, KOREA; 2) Insect ResourcesLaboratory, KRIBB, Daejeon, KOREA; 3) Laboratory of Human Genomics, KRIBB,Daejeon, KOREA.

PHYSIOLOGY AND AGINGWilliamStaatz

963BRegulation of SOD by LAMMER kinases. William Staatz, Sarah Wilkinson,Emmanuelle Meuillet. Arizona Cancer Ctr, Univ Arizona, Tucson.


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CELL DIVISION AND GROWTH CONTROL880CThe condensin subunit CapH2 ensures faithful separation of male meiotic chromosomes. Tom Hartl, SarahSweeney, Paula Campbell, Giovanni Bosco. Dept Molec & Cellular Biol, Univ Arizona, Tucson, AZ.

Condensins I and II are multi-subunit protein complexes that are implicated in chromosome condensation and

faithful chromosome separation each cell cycle. Mutations exist in Drosophilacondensin I subunits gluon/SMC4,CapG, and barren/CapHthat lead to extensive failure in mitotic chromosome separation in embryonic and/or larvalbrain cell divisions. We have isolated four mutant alleles of the condensin II subunitCapH2, three of which arespecifically male sterile and one weaker allele that causes male specific non-disjunction. Cytology of primaryspermatocytes fromCapH2mutant males clearly shows a high degree of chromatin disorganization and uponanaphase, chromosomes do not become completely separated while migrating to the poles. Although male meiosisis disrupted in CapH2mutants, females may have no significant consequence as fertility is only subtly altered andnon-disjunction has yet to be observed. Females do have one striking phenotype, the chromosomes in theirpolyploid nurse cell nuclei become highly polytene throughout the life of the nurse cell. In Xenopusand humantissue culture cells it has been shown that a distinct condensin complex exists that is made up of non-SMC subunitsCapD3, CapG2, and CapH2. It is likely that CapH2 and CapD3 also act together in flies as part of a condesin IIcomplex because like CapH2mutants, flies homozygous for a CapD3mutant allele are also male sterile and carrypolytene chromosomes in their nurse cell nuclei. We propose that CapH2 and CapD3 act as part of a Drosophila

condensin II complex that functions in male meiosis to mediate disjoining of chromosomes upon anaphase onset.In addition, this complex is necessary to resolve polytene chromosome attachments and/or prevent their formationduring nurse cell development.

881AA functional genomics screen identifies Mat89Bb as a novel cell cycle regulator. Michael Anderson, Laura Lee.Dept Cell & Developmental Biol, Vanderbilt Univ, Nashville, TN.

Early embryonic cell cycles in Drosophila consist of rapidly alternating rounds of DNA replication (S phase) andmitosis (M phase) without intervening gaps (G1 and G2). Driven by large maternal pools of RNA and protein, thesestreamlined cell cycles are regulated by posttranscriptional mechanisms. Three Drosophila genes, pan gu(png),plutonium(plu), and giant nuclei(gnu), play crucial roles in coordinating these rapid S-M cycles. Mutation of any ofthese three genes disrupts proper coupling between S phase and mitosis, resulting in DNA replication in theabsence of mitosis with the accumulation of polyploid nuclei in embryos from homozygous mutant females. Thisgiant nuclei phenotype can be explained, at least in part, by decreased levels of mitotic cyclins in mutant embryos.

The pnggene encodes a serine/threonine kinase, and pluand gnuencode novel proteins. We have previouslyshown that proteins encoded by these three genes physically interact to form an active PNG kinase complex.

We previously performed a genome-scale biochemical screen for PNG kinase substrates that led to theidentification of Mat89Bb, a novel, maternally expressed protein of unknown function. Knockdown of Mat89Bbfunction in Drosophila embryos by RNAi resulted in a weak giant nuclei phenotype, and knockdown of the Mat89Bbhomolog in Xenopus embryos by morpholinos similarly resulted in both cell cycle defects (polyploidy) anddevelopmental arrest. Furthermore, we have also shown that human Mat89Bb is required for somatic cell cycleregulation. These findings have revealed that Mat89Bb plays a critical, conserved role in regulating both the cellcycle and development. Current efforts are directed towards the identification and characterization of DrosophilaMat89Bb mutant lines. A careful phenotypic analysis of these mutants will likely have relevance for ourunderstanding of Mat89Bbs cell-cycle and developmental functions in Drosophila as well as higher organisms.

882BA role of histone chaperon ASF1 and Tousled-like kinase in cell cycle progression. Maxim Pilyugin1, Yuri Moshkin2,Franois Karch1. 1) University of Geneva, Switzerland; 2) Erasmus University Medical Centre, Netherlands.

ASF1 is highly conserved histone chaperon. We have investigated the biological function of ASF1 in control ofchromatin dynamics and cell cycle progression using Drosophila as a model organism. We identified two mutationsin asf1 gene that appeared to suppress heterochromatin-mediated silencing, demonstrating a role for ASF1 in theproper assembly of silenced chromatin. We have performed genetic interactions experiments that led us to discoverthat chromatin assembly factor ASF1 cooperates in vivo with the Brahma ATP-dependent chromatin remodelingmachinery. We also performed ASF1 RNAi knockdown study in Drosophila cell culture. The global changes of gene


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expression in ASF1 depleted cells were analyzed mRNA hybridization on Affymetrix GeneChip array and comparedto the changes caused by depletion of BRM. Statistically significant correlation of the gene expression changes hasbeen found in the two sets of data.

We showed that ASF1 is a phosphorylation target of cell cycle regulated Tousled-like kinase (TLK). The analysisof DNA content in TLK RNAi treated cells implies that the reduction of TLK activity slowdown the transition from G1to S phase. Our data suggest as well that TLK activity affects ASF1 protein stability providing a mechanism forASF1 function regulation.

As a histone chaperone, ASF1 may influence a chromatin structure of genes and affect their expression. Ourresults suggest that high level of ASF1 may exacerbate regulation by E2F in vivo. The comparison of geneexpression changes in Drosophila cell depleted of E2F complex components, ASF1, TLK, and BRM implies the rolefor ASF1 and BRM in transcriptional regulation of the genes controlled by E2F and suggests that ASF1 acts as aco-activator for E2F1 regulated genes with assistance of BRM. Therefore, both in vivo and in vitro experimentssuggest that E2F and ASF1 are acting together in the regulation of E2F target genes via the SWI/SNF complex.

883CMisato is required for centrosome separation in both mitosis and male meiosis. Violaine Mottier, Fiammetta Verni,Giovanni Cenci, Maurizio Gatti, Silvia Bonaccorsi. Genetica e Biologia Moleculare, Universita di Roma La sapienza,Roma, ITALY.The Drosophila misato (mst)gene encodes a protein that contains motifs shared among tubulins, as well as a

motif related to the myosin heavy chain. Previous studies showed that the mstmutant alleles mstLB20and mstC27are

late lethal and exhibit frequent polyploid cells in larval brains (Miklos et al., 1997). However, the precise function ofthe Misato protein remains unknown. Sequencing of the mstgene in the LB20and C27mutant alleles shows thatboth mutations lead to truncated proteins. Examination ofmstmutant brains reveals that most mitotic spindles(70%) are monopolar, suggesting a defect in centrosome separation. In addition, these monopolar spindles displayshorter and fewer microtubules than wild type spindles. Nevertheless, recruitment of the centrosomal proteins CNN,-tubulin, D-TACC, CP190, CP60, DGRIP91, DPLP is not affected inmstmutants. mstmutants do not show majordefects during the first meiotic division but display frequent spindles (67%) with unseparated centrosomes duringthe second division. These findings can be explained considering that the first meiotic division is considerablylonger than the second, giving the centrosomes enough time to separate from each other. Using a monoclonalantibody raised against Misato, we find that this protein localizes at the spermatid basal body, which is acentrosome-derived structure. However, no centrosomal localization is observed in dividing cells. We aregenerating flies expressing a Misato-GFP fusion protein to determine whether Mst is enriched at mitotic and meioticcentrosomes.

884ACharacterisation of ZW10 in Cytokinesis. Alan Wainman, Maria Grazia Giansanti, Michael Goldberg, Maurizio Gatti.Genetica e Biologia moleculare, Universita di Roma La Sapienza, Roma, ITALY.

ZW10, along with the other member of the Rod, Zwilch, Zw10 (RZZ) complex, are required for the properfunctioning of the mitotic spindle checkpoint. In addition to this well characterized role, the male meiotic divisions ofzw10mutants display defects in cytokinesis, whereas rodand zwilchmutants show no cytokinesis defects. Here wedemonstrate that all three RZZ components concentrate within the spindle envelope remnant during late anaphase,and during telophase aggregate to form a band across the mid-zone of the spindle envelope. We also present aphenotypic analysis ofzw10mutants demonstrating that cytokinesis failure is similar to that observed in giotto, fourwheel driveand four way stopmutants. These results suggest a role for ZW10 in mediating membrane dynamicsduring cytokinesis, consistent with recent findings indicating the human homologue of ZW10 is involved in Golgitrafficking.

885BMechanisms and effects of cell death in Minute-induced cell competition. Wei Li, Nicholas E. Baker. Dept. ofMolecular genetics, Albert Einstein College of Medicine, Bronx, NY 10461.

Cell competition has been reported to play important roles in growth regulation and organ size control. Toinvestigate the mechanisms and effects of cell death during cell competition, we examined extensive interfaces ofcompeting populations when +/+cells were generated by mitotic recombination in M/+backgrounds. We found thatcell death in cell competition happens only at specific locations and that such characteristic cell death is required forcell competition. We focused on such site specific cell death to study the roles of cell intermingling and Dppsignaling in competition. Both are affected by the cell death. The enhanced growth that cell competition induces in


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the +/+cells was also studied. We found that such enhanced growth depended on death of M/+cells and differedmechanistically from compensatory cell proliferation that has been reported in other situations. We are currentlystudying genes that are required for cell competition and the possible role of phagocytosis in the process.

886CThe role of the gene white in increase of mosaic clone frequency in D. melanogaster and D. simulans. RomanSidorov1, Elena Ugnivenko2, Kirill Kirsanov2, Elizabeth M. Khovanova2. 1) Inst Carcinogenesis, Cancer Research

Center RAMS, Moscow, Moscow Region, RUSSIAN FEDERATION; 2) Koltzov Institute of Developmental BiologyRAS, Moscow, Moscow Region, RUSSIAN FEDERATION.In flies heterozygous for white and other X-linked markers the marker linked to the white mutation in cis-,

possesses higher mosaic clone frequency than the marker in trans-. E.g., in y ++/ +w sn heterozygotes the singedclone frequency is higher than the frequency of the twin yellow clones. This effect is true in two Drosophila species,D. simulans and D. melanogaster, for both spontaneous and induced by various agents (-irradiation, chemicalmutagens, H+-factor of genetic instability) somatic mosaicism. The effect is more obvious for small clones. Itdepends upon the irradiation dose and developmental stage at which the mutagen was applied.

887AA Protein Interactin Map Guided Screen for Novel Regulators of the Cell Cycle. Stephen T. Guest1, Maria A.Cypher1, Russell L. Finley J r.1, 2. 1) Center for Molecular Medicine and Genetics; 2) Department of Biochemistryand Molecular Biology, Wayne State University School of Medicine, 540 East Canfield Ave, Detroit Michigan 48201,

USA.Large-scale protein interaction maps (PIMs) have now been generated for several model organisms includingDrosophila melanogaster.These maps contain many previously identified interactions between members ofcharacterized protein complexes and signaling pathways. The maps also reveal a vast number of novelinteractions, including many involving uncharacterized proteins. These interactions illuminate potential novelplayers in critical cellular processes. We have performed network analysis of the currently available PIM data forDrosophilain search of interactions that identify potential novel regulators of the cell cycle. Our analysis hasidentified two high confidence subsets of proteins that are involved in novel interactions with known cell cycleregulators. Proteins in the first subset are involved in novel interactions with members of the cyclin dependentkinase family, while proteins in the second subset are involved in novel interactions with members of the SCFubiquitin ligase complex. To identify a role for these proteins in cell cycle progression, we reduced their expressionin cultured Drosophilacells by RNA interference in a 96-well format and looked for cell cycle defects using flowcytometry. As a result of this approach, we have identified several novel regulators of cell cycle progression. Ourresults validate the use of PIM data in guiding discovery of novel regulators of key cellular processes.

*S. Guest and M. Cypher contributed equally to this work.

888BThe Regulation of the Tumor Suppressor Activity, PTEN by Thioredoxin Controls Cell Number and Cell Size. ZuoheSong1,2, Negin Saghafi1, Marc Brabant1,3, Emmanuelle Meuillet1,2,3. 1) Arizona Cancer Ctr, Univ Arizona, Tucson,AZ; 2) Nutritional Sciences Department, University of Arizona, 1177 E. 4th Street, Tucson, AZ. 85721, USA; 3)Molecular and Cellular Biology Department, University of Arizona, Tucson, AZ. 85724, USA.

Human Thioredoxin-1 (hTrx-1) is a redox protein with a molecular weight of 12 kDa, which contains the twocatalytic site cysteine residues -Trp- Cys32-Gly-Pro-Cys35-Lys found in all thioredoxin proteins. hTrx-1 has beenreported to play an important role in cell growth, apoptosis, and cancer patient prognosis. Recently, we havedemonstrated that hTrx-1 binds to the C2 domain of hPTEN in a redox dependent manner. This binding leads tothe inhibition of PTEN lipid phosphatase activity in mammalian systems (1). In this study, we show that over-expression of hTrx-1 in Drosophila Melanogaster promotes cell proliferation during eye development as measured

by eye size and ommatidia size. Furthermore, hTrx-1 can rescue the small eye phenotype induced by the over-expression of the tumor suppressor gene PTEN. We demonstrate that hTrx-1 rescue of the PTEN overexpressioneye size phenotype requires cysteine218 in the C2 domain of PTEN. In addition, we show that hTrx-1 expressionresults in increased Akt phosphorylation supporting our conclusion that he hTrx-1 induced eye size increase resultsfrom the inhibition of the PTENs PtdIns-3-phosphatase activity. Our study confirms the redox regulation of PTENthrough disulfide bond formation with the hTrx-1 in Drosophila and suggests a conserved mechanisms for

Thioredoxins and their interactions with the PtdIns-3-kinase signaling pathway in man and the fruit fly.


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CYTOSKELETON AND CELLULAR BIOLOGY889CRegulation of autophagosome formation by paxillin during nutrient stress and development. Guang-Chao Chen1,3,Sheila Thomas2, J effrey Settleman1. 1) MGH Cancer Center, Charlestown, MA; 2) Beth Israel Deaconess MedicalCenter and Harvard Medical School, Boston, MA; 3) Inst of Biological Chemistry, Academia Sinica, Taipei,

TAIWAN.

We have previously shown that Drosophila paxillin functions in regulation of Rho GTPases in tissuemorphogenesis (Chen et al. 2005, Mol Cell Biol). In order to further elucidate its role in development, we undertooka misexpression screen to isolate new functional partners of paxillin. Wing-specific expression of paxillin inducesblistered wings, and this phenotype was used as the basis for a modifier screen of ~1500 EP lines. One of thecandidates identified corresponds to the serine/threonine kinase Center divider (Cdi, EP3319), a homolog ofDrosophila LIM kinase, which is involved in the regulation of the actin cytoskeleton via cofilin. Furthermore, theinsertion EP(3)3348 in the 5UTR of Drosophila Ulk was isolated as a strong suppressor of the paxillin-induced wingblistering phenotype, but has no effect on the Dlimk-induced wing phenotype. The dUlk mutant generated by the Pelement excision of EP3348 fails to suppress the paxillin-induced wing phenotype, suggesting that dUlk may be aspecific interactor with paxillin. Ulk is involved in autophagosome formation and axon outgrowth. In Drosophila,ecdysone receptor signaling activates programmed autophagy. Interestingly, ecdysone receptor mutationssuppress paxillin induced wing phenotype. We are currently investigating the role of paxillin in autophagosomeformation and neuronal differentiation in development.

890ARegulation of Cell Shape During Eye Organogenesis. Douglas Corrigall, Franck Pichaud. MRC Laboratory forMolecular Cell Biology, UCL, London, UNITED KINGDOM.

Control of cell shape has been shown in many diverse metazoan phyla to be crucial to the proper development oftissues and organs. This cell response is often polarized and by definition involves rearrangement of the F-actin/microtubule cytoskeleton downstream of patterning cues. To address this problem, we are using the strikingapical cell constriction in the fly eye that is associated with the morphogenetic furrow (MF) downstream of theconserved Dpp and Hh pathways. We have initiated a pilot screen using available FRT lines corresponding to asubset of the cytoskeletal-related factors identified as regulators of cell shape in an S2 cell based system (Kiger etal. 2003). This screen demonstrates that i) we can detect robust phenotypes affecting the MF cell response, and ii),only a minority of these factors might be relevant in this process. In particular we will present evidence that loss-of-function clones of the cofilin-phosphatase slingshot (ssh) give a striking phenotype in the MF, in whichhyperaccumulation of F-actin is consistent with a failure to inhibit cofilin activity and results in loss of the MF cellresponse and prevention of proper neuronal differentiation.

891BThe role of Planar Cell Polarity Effector genes in the embryonic epidermis. Masyasu Hirano1, J anie Coe1, ObianujuDike1, Nan Ren2, Paul Adler2, Simon Collier1. 1) Dept Biological Sci, Marshall Univ, Huntington, WV; 2) Dept.Biology, University of Virginia, VA.

During late embryogenesis the epidermal epithelium becomes patterned with polarized structures. Rows ofdenticles appear on the ventral side and the dorsal surface becomes almost entirely covered in cell hairs. ThePlanar Cell Polarity (PCP) Effector genes, fritz, fuzzy, inturnedand multiple wing hairsare required for the correctspacing, orientation and number of these structures. Our analysis of PCP Effector gene mutant phenotypes revealsthat these genes control epithelial cell shape, cell polarity and the number of denticle or hairs produce per cell.Changes in F-actin distribution in PCP Effector mutants and the requirement for small GTPase function suggeststhat the regulation of actin cytoskeleton is critical for embryonic epidermal patterning. Significantly, a Fritz-GFP

fusion protein localizes with F-actin throughout the developing epidermal epithelium. We propose a three-stepmodel for epithelial patterning that requires the coordinated control of cell shape, cell polarity and the formation ofcell structures. All three steps are mediated by the actin cytoskeleton under the regulation of the PCP Effectorgenes.

892CRegulation of epithelial cell-cell adhesion during wing development in Drosophila. Manish J aiswal, Pradip Sinha.Bio Sci & Bioengineering, Indian Institute Technology, Kanpur, INDIA.

In a developing organ, intercellular adhesive interactions are involved in sorting and aggregation of cells.Expression and distribution of cell adhesion proteins involved in these interactions are often regulated by instructivecues from the signaling pathways involved in pattern formation and growth. Cell adhesion proteins in turn alsocoordinate cell-cell communication. A tight coordination between cell-cell adhesion and growth/pattern regulation


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thus determines the characteristic size and shape of an organ. In Drosophila, the primordia of the adultappendages i.e., imaginal discs, offer an elegant model to investigate these cellular and developmentalmechanisms. Here, we show that the Wg/Wnt and Dpp signaling that regulates growth and patterning of wingimaginal disc also regulates cell-cell adhesion. Both Wg and Dpp signaling provides cues for developmentalregulation of DE-Cadherin (DE-Cad) which codes for a homophilic cell adhesion protein. Our results reveal that theWg signaling mediated regulation of cell adhesion is a function of its transcriptional output rather than a directinteraction of Wg signaling induced elevated Arm/-catenin pool with that of DE-cadherin at the adherence junction.

We further show that Fat (Ft), a large cadherin-like protein involved in heterophilic cell-cell adhesion, geneticallyintersects with the Wg pathway inhibits DE-Cad transcription. The regulation of spatial pattern of cell-cell adhesionand remodel the epithelial cell-cell junctions in the growing wing imaginal disc that determines the final shape of theadult wing.

893AA role for the Tuberous Sclerosis Complex during photoreceptor apical membrane differentiation. Ella Palmer,Franck Pichaud. Anatomy and Developmental Biology, UCL. MRC LMCB & CBU, Gower Street, London. WC1E6BT. UNITED KINGDOM.The vast majority of cancer in humans originate from epithelia. In order to better understand the nature of the

cytoskeletal and polarity instabilities that could lead to tumorogenesis we are using the genetically amenabledeveloping photoreceptor as a model epithelial cell. Completion of the Drosophilagenome has led to theidentification of approximately 1000 genes involved in cytoskeleton dynamics and these genes are being screened

using FRT chromosomes carrying the mutations of interest and in vivoRNAi. We report here the results from a pilotrecessive screen that was performed on the right arm of the third chromosome. Among the genes that wereexamined, we have identified Tuberous Sclerosis Complex 2 (TSC2), an important regulator of cell growth, as a keyfactor for apical membrane morphogenesis. In absence of this gene function, the morphogenesis of the apical lightgathering organelle of the photoreceptor is strongly impaired suggesting that the TSC1 and TSC2 genes play a rolein regulating this differentiation process in photoreceptors.

894BMotors and Morphogenesis: Role of Dynein and Dynactin in testicular fusome assembly in Drosophila. KrishanuRay, Anindya Ghosh-Roy, Rishita Chengede, Madhura Kulkarni. Dept. of Biological Sciences, Tata Inst. Fund. Res.(TIFR), Mumbai, Maharashtra, INDIA.

Fusomes are tubulovesicular organelles present in the germ line cysts of holometabolous insects. Studies inDrosophilaovary established that it is rich in spectrin, adducin (Hts) and other spectrin-associated proteins, and it isconnected to the endoplasmic reticulum through rapid exchange of membrane. Fusomes contain the microtubule-organizing center (MTOC) and determine the asymmetric cell divisions as well as the oocyte cell fate in the ovary.In comparison, very little is known about the composition and role of fusome in male germ-line cysts, whichdifferentiates symmetrically to produce sixty-four identical sperm. We find that the Dynein Light Chain 1 (DLC1),along with spectrin and adducin, is enriched in testicular fusomes and loss of the protein in ddlc1 hemizygoustestes affect the fusome assembly. In addition, the results of a genetic interaction analyses suggest that both theintermediate chain subunit (IC74, sw1) of the cytoplasmic dynein and the P150dynactin (Glued) are required for thetesticular fusome assembly. They are required for DLC1 localization to the organelle. Altogether, these results haveprovided a new insight into the mechanism of fusome assembly in particular and the endomembrane organizationin general in Drosophila.

895CIn vivo analysis of Drosophila ventral furrow formation. Florian Ulrich, Eric Wieschaus. Dept Molecular Biol,Princeton Univ, Princeton, NJ .

During Drosophilaventral furrow (VF) formation, mesodermal precursors separate from the prospectiveneurectoderm through a sequence of rapid cell shape changes, including apical flattening and constriction, cellelongation and subsequent shortening, leading to the internalization of the cells along the anterior-posterior axis.VF formation is induced by the patterning genes dorsal and twist that regulate the expression offolded gastrulation(fog). The secreted Fog protein localizes myosin II towards the apical side of prospective mesodermal cells via apathway involving RhoGEF2 and DrosophilaRho-associated kinase (Drok). Myosin II interacts with actin andadherens junctions to constrict the cells on their apical sides and drive them into the embryo. In vivostudies of VFformation partly suffer from the light scattering nature of the tissue especially deep within the embryo. As a result,most of our knowledge about the functions of the genes regulating mesoderm internalization relies on antibodystaining on fixed sections. Little is known about the forces and cell-biological mechanisms that dynamically regulatemesoderm internalization in vivo. Here, we report the development of an imaging-based assay to analyze ventralfurrow formation in vivo. Drosophilaembryos with fluorescently labeled intracellular compartments such as nucleus,


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membrane, junctions and cytoskeletal elements can be recorded in high spatial resolution over time by three-dimensional multi-photon microscopy. The morphology of cells as well as the distribution of subcellular markersover time can be analyzed around 150 m deep within the embryo. This assay can be applied to mutant embryosand embryos, in which candidate cell-biological mechanisms have been impaired, to elucidate the molecular andcellular principles that drive mesoderm internalization in vivo. In principle, it should also be possible to adapt thisassay to other morphogenetic processes in the embryo, such as the formation of the cephalic furrow or theposterior midgut.

896ACadherin-catenin complex regulates plasma membrane localization of the exocyst complex component Sec6.Slobodan Beronja, Ulrich Tepass. Department of Zoology, University of Toronto, Toronto, ON, CANADA.The multiprotein exocyst complex, consisting of Sec3, Sec5, Sec6, Sec8, Sec10, Sec15, Exo70 and Exo84, has

been shown to function in polarized exocytosis in yeast, Drosophilaand vertebrate cell cultures. The exocyst actsas a tethering complex for the incoming secretory vesicles, and it is thought that by virtue of its restrictedlocalization, the complex acts to spatially control delivery of new membrane. What controls the localization of theexocyst complex is not clear. Interactions between the apical junctional complexes and the exocyst complex havebeen shown in both vertebrate cell cultures and in Drosophila. The main apical junctional complex of the Drosophilaepithelium is the adherens junction, components of which are the transmembrane molecule DE-cadherin (DEcad),which through homophilic interaction mediates adhesion between neighboring cells, and the cytoplasmic D-catenin and Armadillo, which link DEcad to the actin cytoskeleton. The Drosophilagenome contains two other

classic cadherins: DN-cadherin (DNcad), which is largely restricted to the CNS and the non-essential DN-cadherin2, which can function redundantly with DNcad. DNcad has been identified as a mediator of photoreceptorneuron targeting in the brain, and is essential for establishment of correct neuronal connections. A recent study hassuggested a surprising function of the exocyst complex in the targeting process, raising the possibility that theexocyst complex functionally interacts with DNcad. In this study we are investigating the nature and functionalsignificance of the interaction between Sec6 and the classic cadherins.

897BEndocytic control of wing development in Drosophila m. Giovanna Mottola1,2, Eric Marois1, Suzanne Eaton1,Marcos Gonzlez-Gaitn1, Marino Zerial1. 1) Max Planck Institute for Cell Biology and Genetics, Dresden,Germany; 2) Dipartimento di Biochimica e Biotecnologie Mediche, Universita' di Napoli Federico II, Napoli, Italy.

Endocytosis is crucial to control cell-surface receptors and the magnitude, duration and specificity of signalingevents. In the past years how endocytosis modulates signaling has been investigated mainly in cultured cells orusing in-vitro cell-free systems. We want to address this question in the context of an organism such Drosophila m.We focused on the small GTPase Rab5, a key regulator of several steps of endocytosis: internalization of endocyticvesicles at the plasma membrane, fusion of these vesicles with early endosomes, early endosome biogenesis andmotility. Our group has demonstrated that the multi-functionality of Rab5 is due to its ability to recruit and regulatemore than 40 effectors, creating defined membrane domains. In order to follow specific Rab5-dependent endocyticsteps during the development of Drosophila wing, we have explored the function of two Rab5 effectors,Rabenosyn5, already characterized in mammalian cells, and p95, one of the subunits of a novel complex. In thisstudy we show that although part of the same machinery, Rabenosyn5 and p95 have different functions indevelopment. Loss of Rabenosyn5 by knock out leads to lethality during first instar larval stage. Rabenosyn-5clones are slow-growing and eliminated from the wing imaginal discs. Overexpression has also dramatic effects onthe growth and patterning of the wings, which are even more severe, when apoptosis is blocked. These datahighlight the relevance of Rabenosyn5 in regulating endocytosis and cell survival. On the contrary, overexpressionand knock down by RNAi of p95 in Drosophila induce strong defects in wing veins formation. Analysis byimmunofluorescence and confocal analysis revealed changes in the EGF dependent-activation of MAPK cascade.

Other signaling pathways are not affected. Our data suggests that this novel complex has a specific involvement inthe regulation of EGF receptor trafficking and/or signaling.

898CControl of Neuronal Morphogenesis and the Delta/Notch Signaling Pathway by Shrub, a Novel Coiled-Coil Proteinin Drosophila. Neal T Sweeney1, 2, J ay E. Brenman3, Yuh Nung J an2, 4, Fen-Biao Gao1, 2, 5. 1) Gladstone Institute ofNeurological Disease at UCSF, San Francisco, CA; 2) Neuroscience Program, UCSF, San Francisco, CA; 3)Department of Cell and Developmental Biology and Neuroscience Center University of North Carolina,


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Chapel Hill, NC; 4) Department of Physiology and Howard Hughes Medical Institute, UCSF, San Francisco, CA;5) Department of Neurology, UCSF, San Francisco, CA.

Dendritic branching is a complex process controlled by many signaling pathways, including Notch. Here we reportthe identification of mutations in the shrub gene that increased dendritic branching and enhanced signaling by theNotch pathway. Single-cell clones of shrub mutant multiple dendritic sensory neurons in Drosophila larvae showedectopic dendritic and axonal branching in neurons, indicating a cell-autonomous function in neuronalmorphogenesis. Shrub encodes an evolutionarily conserved coiled-coil protein homologous to the yeast protein

Snf7, which is involved in the formation of a subset of late endosomal compartments known as multivesicularbodies. Accordingly, we found that mouse orthologs could substitute for Shrub in mutant Drosophila embryos. Lossof Shrub function caused abnormal distribution of several endosomal markers. Shrub mutant embryos also hadelevated expression levels of processed Notch C-terminal fragment and a fragment of Notch ligand Delta, as wellas Notch-dependent transcription. Further genetic studies revealed cell-autonomous functions for Notch and Deltain promoting dendritic branching. These data support a model in which control of dendritic morphogenesis by Shrubinvolves endosomal regulation of the Delta/Notch signaling pathway.

899ADomain-specific early and late function of Dpatj in Drosophila photoreceptor cells. Sang-Chul Nam, Kwang-WookChoi. Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030.The formation and maintenance of cell polarity is essential for epithelial morphogenesis. Dpatj (Drosophila

homolog of mammalian Patj) is a multi-PDZ domain protein that localizes to the apical cell membrane and forms a

protein complex with cell polarity proteins, Crumbs (Crb) and Stardust (Sdt). While Crb and Sdt are known to berequired for the organization of adherens junctions (AJ s) and rhabdomeres in differentiating photoreceptors, the invivo function of Dpatj as a member of the Crb complex in developing eye has been unclear due to the lack of loss-of-function mutations specifically affecting the dpatj gene. Our genetic analysis of hypomorph, null and RNAinterference reveals distinct dual functions of Dpatj in developing and mature photoreceptors. The C-terminal region(PDZ domains 2-4) of Dpatj is not essential for development of the animal but is required to prevent late-onsetphotoreceptor degeneration. In contrast, the N-terminal region of Dpatj is essential for animal viability andphotoreceptor morphogenesis during development. The localization and maintenance of Crb and Sdt in the apicalphotoreceptor membrane are strongly affected by reduced levels of Dpatj. Dpatj is necessary for proper positioningof AJ s and the integrity of photoreceptors in the developing retina as well as for the maintenance of adultphotoreceptors. Our study provides evidence that Dpatj has domain-specific early and late functions in regulatingthe localization and stability of the Crb-Sdt complex in photoreceptor cells.

900BThe role of phosphatidylinositol 4-kinase III in development. J ulie Tan1,2, J ulie Brill1,2. 1) Developmental Biology,Hospital for Sick Children, Toronto, ON CANADA; 2) Molecular and Medical Genetics, University of Toronto,

Toronto, ON CANADA.Phosphoinositides (PIPs) are involved in many fundamental cellular processes, including actin organization,

membrane trafficking and cell signaling. Phosphatidylinositol 4-kinases (PI4Ks) phosphorylate the D-4 position ofthe inositol ring of phosphatidylinositol (PI) to yield PI4P. PI4P can be further phosphorylated to yield other PIPssuch as PI(4,5)P2 and PI(3,4,5)P3. Whereas PI(4,5)P2 and PI(3,4,5)P3 are recognized as important molecules of thecell, PI4P itself is emerging as a key player in cellular trafficking, secretion and signaling.Drosophilahas three PI4Ks, PI4KII, PI4KIII, and PI4KIII/Fwd. Of these, only Fwd has been characterizedgenetically. Fwd is required only for the completion of cytokinesis in male meiosis. fwdmutants are male sterile butviable, indicating that the other PI4Ks likely play essential roles in other tissues during development. AlthoughPI4KIII is essential in budding yeast, where it plays roles in cell wall integrity, vacuole morphology and actinorganization, the function of P I4KIII has never been studied in a multicellular organism. My long-term goal is to

characterize the effect of mutations in PI4KIII on cell growth and signaling during development.Using P-element mutagenesis, I generated a deletion in the PI4KIII gene (CG10260)that removes the last 33amino acids of the predicted catalytic kinase domain and results in lethality. I am designing rescue constructs toconfirm that lethality is due to loss of PI4KIII. Also, I am using another deletion that brought the P-element closerto PI4KIII to screen for larger deletions predicted to be protein null. Future directions include dissecting the tissuespecificity, molecular function and genetic interactors of PI4KIII which together will uncover the biological role ofPI4KIII and PI4P in development.


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GENOME AND CHROMOSOME STRUCTURE901CCHD1: a chromodomain-containing chromatin remodeling factor. J ennifer A. Armstrong, Matthew S. Berger,

J ennifer M. Lee, Ivy E. McDaniel, Nick L. Reeves. J oint Science Dept, Claremont Colleges, Claremont, CA.We are interested in dissecting the relative roles of the many chromatin remodeling factors localized to

transcriptionally active regions. CHD1 is a member of a large family of ATP-dependent chromatin remodeling

factors, including Brahma (BRM) and ISWI. CHD1 co-localizes with elongating RNA Polymerase II (Pol II) on larvalsalivary gland polytene chromosomes, suggesting that CHD1 may facilitate the passage of Pol II throughchromatin. Human CHD1 was recently shown to bind histone H3 methylated on lysine 4 via its chromodomains,while yeast CHD1 was unable to bind methylated H3K4. The tandem chromodomains ofDrosophilaCHD1 aremore similar to those in the human protein, suggesting that histone methylation might recruit CHD1 to active genesinDrosophila. To understand interactions between CHD1 and other chromatin remodeling factors, we are makinguse of eye-based assays designed to identify factors important for the BRM and ISWI chromatin remodelingfactors. Preliminary studies indicate that loss ofbrmmakes cells more sensitive to levels ofchd1. In addition, CHD1localization on polytene chromosomes suggests that its activity may not be limited to Pol II genes. We findmoderate levels of CHD1 in the nucleolus during normal larval growth, and high levels following heat shock,suggesting that CHD1 may be involved in transcription of rRNA genes.

902ADeciphering chromatin based cellular processes in development using a dominant negative histoneacetyltransferase.Meridith Toth, Xianmin Zhu, Neetu Singh, Felice Elefant. Dept Bioscience/Biotechnology, DrexelUniv, Philadelphia, PA.

DNA is packaged into nucleosomes around histone protein cores so tightly that post-transcriptional modificationsare necessary to allow gene expression to proceed. Targeted gene expression which is critical in differentiation anddevelopment is made possible by one such modification, acetylation, which is associated with active gene domains.Acetylation is catalyzed by histone acetyltransferases (HATs), proteins that transfer the acetyl group from acetyl co-A to conserved lysine residues on histone protein tails. Misregulation of HATs early in development has implicatedthem in various neurodegenerative diseases and cancers. The goal of this study is to understand the specificdevelopmental implications that a particular HAT protein plays in eukaryotic development using aDrosophilamodelsystem. Our HAT of interest is DrosophilaHAT Tip60 (dmTip60), a specific human HAT homologue found by ourlab through database searches. Alignments with the human homologue showed dmTIP60 to be56%identical/68%similar, making it a good candidate for ultimately relating our findings to the human system. Wehave chosen this HAT because it is essential in cell cycle progression, is implicated in disease states includingAlzheimers Disease and various cancers, has been directly associated with prostate cancer, but has not yet beenstudied in a multicellular developmental model system. We will be considering the developmental significance ofthis protein through the generation of dominant negative mutations, which will be expressed in vivousing aGAL4/UAS inducible system in Drosophila. The use of dominant negative mutations will allow us to differentiatebetween functions that are complex related and those that are based on the HAT activity of Tip60. We expect thattissue-specific production of these proteins during Drosophilaembryogenesis will lead to severe phenotypicchanges, and in future experiments the genes associated with these changes can be determined.

903BA dominant negative form of the BEAF insulator proteins disrupts chromatin structure. Craig M. Hart, MatthewGilbert, Swarnava Roy, Yian Yee Tan. Dept Biological Sciences, Louisiana State Univ, Baton Rouge, LA.The division of chromosomes into discrete functional domains in the three dimensional space of the nucleus is

thought to play an important role in the regulation of gene expression. The boundaries of domains are thought to

actively defined by specialized DNA sequences known as insulator (or boundary) elements. In transgene assays,insulators prevent interactions between enhancers and promoters when inserted between them. Insulators alsobuffer bracketed transgenes against chromosomal position effects. Binding sites for the Boundary Element-Associated Factor BEAF are necessary for the insulator activity of the scs insulator in transgenic flies. BEAF bindsto hundreds of interbands on polytene chromosomes, indicating that BEAF-utilizing insulators are common inDrosophila. BEAF is comprised of complexes of two 32 kDa proteins (BEAF-32A and 32B) that are derived from thesame gene, and differ only in their DNA binding domains. 32A and 32B interact with each other via a carboxy-terminal domain, but do not form stable complexes with other proteins. We have made transgenic flies with atransgene encoding the BEAF self-interaction domain (BID) which is under GAL4 UAS control. We provide


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evidence that the BID protein functions as a dominant negative form of BEAF. In support of models that proposea relationship between insulator function and chromatin, results will be presented that show that BID affectschromatin structure or dynamics.

904CIdentification and Characterization of Gypsy-like Endogenous Insulators in Drosophila melanogaster. EdwardRamos, Kelly Baxter, Victor Corces. Dept of Biology, J ohns Hopkins University, Baltimore, MD.

Chromatin insulators have been implicated in the regulation of higher-order chromatin structure and may functionto compartmentalize the eukaryotic genome into independent domains of gene expression. To test this possibility,we used biochemical and computational approaches to identify gypsy-like genomic binding sites for the Suppressorof Hairy-wing [Su(Hw)] protein, a component of the gypsy insulator. The gypsy insulator has long been known toprevent enhancer promoter communication but most studies done use the insulator initially found in the gypsyretrotransposon rather than endogenous binding sites. To increase our knowledge of insulators in the Drosophilagenome, we set out to characterize endogenous gypsy-like Su(Hw) binding sites. EMSA and FISH analysessuggest that these newly identified gypsy-like insulators are genuine Su(Hw) binding sites and thus function asbona fide insulators. The insulator strength is dependent on the genomic location of the transgene and the numberof Su(Hw) binding sites, with clusters of 2-3 sites showing a stronger effect than individual sites. These clusters ofSu(Hw) binding sites are mostly located in intergenic regions or in introns of large genes, an arrangement that fitswell with their proposed role in the formation of chromatin domains. Taken together, these data suggest thatgenomic gypsy-like insulators are capable of regulating gene expression and may provide a means for the

compartmentalization of the genome within the nucleus.905AMapping and mutagenesis of the E(var)3-9 locus. Karen Weiler. Dept of Biology, West Virginia University,Morgantown, WV.

E(var)3-9is a member of a large class of genetic modifiers of PEV identified by mutations that dominantlyenhance the variegation ofwm4. The mutant phenotype suggests a role for the wild-type E(var)3-9 protein inantagonizing heterochromatin formation. E(var)3-9is also required for female fertility.

Initial meiotic recombination and deficiency mapping localizedE(var)3-9to either of two intervals, 85C1-2 to 85D8or 85F6 to 86C1. The results ofPelement-mediated male recombination mapping confirmed that E(var)3-9residedwithin 85C-D but were unable to narrow the target significantly, in part due to ambiguous data. However, theavailability of new deficiencies synthesized using Pelement insertions facilitated the localization ofE(var)3-9to aregion encompassing twenty-three known and predicted genes. The results of additional genetic approaches takento identify the E(var)3-9gene will be described. These include using the FLP-FRT deletion generation system (1)and the P{wHy}deletion-generator system (2) to create novel deficiencies. E(var)3-9was determined to be allelic toCG11971, which is predicted to encode a zinc-finger protein.

1) Parks et al. (2004) Nat Genet36(3):2882) Huet et al. (2002) PNAS99(15):9948.

906BTransmission of Fragment Chromosomes Lacking An Endogenous Telomere. Simon Titen, Kent Golic. Dept Biol,Univ Utah, Salt Lake City, UT.

It was first shown by Herman Muller and Barbara McClintock, in the 1930s and 40s, that the ends of linearchromosomes have distinct properties. An end, or a telomere, is comprised of both protein and DNA thataccomplish two specific functions: 1) Prevent the cell from recognizing the end of the chromosome as a DNAdouble strand break (DSB), which subsequently prevents end-to-end fusions, cell cycle arrest, and interactionsbetween new DSBs and chromosome ends; and 2) Solve the end replication problem.

In order to characterize the mechanisms involved in telomere generation and maintenance our lab has developeda technique to generate chromosomes that lack an endogenous telomere, in vivo, by inducing dicentric bridgeformation using the site-specific recombinase FLP. We have shown that, in the male germ line, these bridgesfrequently break and the two resulting fragments are transmitted to the progeny. Our research has been focused oncharacterizing the molecular structure of these fragment chromosomes and the proteins required for de novotelomere addition and germ line transmission.

907CCharacterizing Drosophila telomeres that lack natural transposons. Xiao-Feng Zheng, Yikang Rong. Lab ofMolecular Cell Biology, National Cancer Institute, Bethesda, MD.

Drosophila telomeres are maintained by targeted attachments of retrotranspons to chromosomal ends, as opposeto telomere elongation by telomerase in most eukaryotes. It is of great interest therefore, to characterize the


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structure and function of Drosophila telomeres, drawing potential similarities to those of popular telomeres.Characterizing Drosophilas natural telomere is unfeasible however, due to sequence heterogeneity at the ends. Tocircumvent this limitation, we created a telomere with a defined sequence by generating a double strand break toeliminate the telomere-associated sequence and retrotransposons. Stocks with this terminally-deleted chromosomecan be stably maintained, even with continuous degradation of DNA at the end. The new ends are sometimeshealed by attachments of transposons. We have initiated structural analysis of this unique end. Preliminary resultssuggest that Drosophila telomeres can also exist in a terminally single-stranded conformation.

908APartially redundant roles of Drosophila ATM and ATR checkpoint kinase for telomere maintenance. Xiaolin Bi1,Deepa Srikanta1, Laura Fanti2, Sergio Pimpinelli2, Yikang Rong1. 1) NCI/NIH, Bethesda, MD,USA; 2) Dipartimentodi Genetica e Biologia Molecolare,Universita di Roma"La Sapienza",Rome,Italy.

In higher eukaryotes, the ataxia telangiectasia mutated (ATM) and ATM and Rad3-related (ATR) checkpointkinases play distinct, but partially overlapping, roles in DNA damage response. Yet their interrelated function hasnot been defined for telomere maintenance. We discover in Drosophila that the two proteins control partiallyredundant pathways for telomere protection: the loss of ATM leads to the fusion of some telomeres, whereas theloss of both ATM and ATR renders all telomeres susceptible to fusion. The ATM-controlled pathway includes theMre11 and Nijmegen breakage syndrome complex but not the Chk2 kinase, whereas the ATR-regulated pathwayincludes its partner ATR-interacting protein but not the Chk1 kinase. This finding suggests that ATM and ATRregulate different molecular events at the telomeres compared with the sites of DNA damage. This compensatory

relationship between ATM and ATR is remarkably similar to that observed in yeast despite the fact that thebiochemistry of telomere elongation is completely different in the two model systems. We provide evidencesuggesting that both the loading of telomere capping proteins and normal telomeric silencing requires ATM andATR in Drosophila and propose that ATM and ATR protect telomere integrity by safeguarding chromatinarchitecture that favors the loading of telomere-elongating, capping, and silencing proteins.

REGULATION OF GENE EXPRESSION909BA mutational analysis of ecdysone receptor and Ultraspiracle interaction in a heterologous cell culture system.Vincent C Henrich, J osh Beatty, J enna Callender. Inst. Health, Science, and Soc, UNC-Greensboro, Greensboro,NC.The ecdysone receptor and the insect RXR homologue, Ultraspiracle (USP) form a heterodimer that mediates

transcriptional activity in the absence and presence of the insect steroid hormone, 20-hydroxyecdysone. Plasmidsencoding these receptors were transfected and expressed in a mammalian cell line that normally shows noresponse to ecdysteroids or juvenile hormone, so that an ecdysteroid response system was reconstituted foranalysis. Several site-directed mutations have been produced for each of the three natural EcR isoforms and twoconstructs of USP, one encoding the DNA-binding domain and the other without it, by measuring their effects onbasal, ecdysteroid-induced, and juvenile hormone potentiated transcriptional activity in cells. The sites wereselected based on known or suspected effects on transcriptional activation functions, cofactor interactions,dimerization, and ligand-binding, using sequence alignments, computational models, and previous studies. Thestudies revealed that some EcR mutations impair specific receptor subfunctions whereas most USP mutations tendto either obliterate activity or exert little effect at all. The analysis indicates that various aspects of EcR/USPtranscriptional activity via the canonical hsp27 ecdysone response element depend upon EcR isoform, thepresence or absence of the USP DNA-binding domain, and specific residues within the USP ligand-binding domain.

910CDisruption of gene function by targeted insertion and inducible RNAi demonstrate nautilus is essential forembryonic myogenesis and viability and impacts founder cell patterning. Qin Wei1, Yikang Rong2, Bruce Patterson1.1) Laboratory of Biochemistry, NCI/NIH, Bethesda, MD; 2) Laboratory of Cellular and Molecular Biology, NCI/NIH,Bethesda, MD.The nautilus gene is the single member of the bHLH family of myogenic regulatory factors in Drosophila. Embryos

injected transiently with nautilus dsRNA displayed severe embryonic muscle disruption indicating nautilus isessential for embryonic muscle formation. In order study nautilus loss-of function throughout development, we usedtwo complementary approaches to inactivate gene function: in the first instance, we used targeted gene disruptionto introduce an armadillo-GFP expression cassette in the middle of the first exon of nautilus gene; in the second,we utilized an inducilbe RNAi transgene to produce tissue-specific expression of nautilus dsRNA under the controlof gal 4. Both the targeted nautilus null and the RNAi transgene produce the same range of muscle defects in the


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embryo, from the severe loss of muscle organization, similar to the RNAi phenotypes observed with the injection ofdsRNA, to minor muscle pattern disruptions. All stages of development are affected: larvae are weak and moveslowly in an uncoordinated fashion, the majority of pupae are unable to exit the pupal case and the smallprecentage that do usually die shortly after hatching. Less than 5% of the homozygous embryos survive to adultsand females are sterile with enlarged abdoments unable to lay eggs. An hsp70 nau-cDNA transgene rescues thenull. nautilus precedes duf expression in founder cells at stage 10 but they are co-exprressed by stage 13. Theembryonic muscle disruption correlates with an abnormal founder cell pattern. These results demonstrate

conclusively that the nautilus gene is required for normal embryonic myogenesis and viability but is not required forthe determination of the myogenic cell lineage.

911AEif1A mutations dominantly suppress the eggshell patterning defect caused by activation of the meioticrecombination checkpoint. Martha Klovstad1, Gail Barcelo1, Uri Abdu2, Trudi Schpbach1. 1) HHMI, MolecularBiology Dept., Princeton University, Princeton, NJ ; 2) Dept. of Life Sciences, Ben-Gurion University.

During early Drosophila oogenesis double-stranded breaks (DSBs) are formed as an early intermediate in meioticrecombination. Analysis of the spindleclass mutants has shown that the persistence of unrepaired DSBs duringDrosophila oogenesis leads to activation of a meiotic recombination checkpoint. Similar checkpoints act in yeast,C.elegans, and mice and result in the induction of apoptosis in mice and C.elegansand in cell cycle arrest in yeast.In contrast, checkpoint activation in Drosophila results in the ventralization of the eggshell and oocyte nuclearmorphology defects. Specifically, checkpoint activation results in the inhibitory modification of the translation factor

Vasa, a protein which is required for translation of the DV patterning ligand Gurken. In order to identify genesinvolved in the meiotic recombination checkpoint we have undertaken an EMS mutagenesis screen on the thirdchromosome for dominant and recessive genetic modifiers of the eggshell defect of mutants in spindleB, a spindleclass gene required for DSB repair. One gene identified as a dominant suppressor is the translation factor,eif1A.Double mutants for spnBand eif1A lay predominately wild-type like eggs. Gurken antibody staining shows thatlocalized Grk protein levels are restored in the majority of double-mutant egg chambers. Eif1A has been implicatedin 80S ribosome assembly, ribosome scanning, and stabilizing the initiator Met-tRNA on the 40S ribosomal subunit.Most notably, Eif1A binds Eif5B in other species and Eif5B has previously been shown to regulate Vasa function.We are currently determining the specificity of the eif1A/spnBinteraction and examining potential functionalinteractions between Eif1A, Eif5B and Vasa .

912BRegulation of Histone Acetyltransferase during Development. Vijayalakshmi Ramakrishnan. Drexel University,Philadelphia, PA.

Histone Acetyltransferases (HATs) are a key class of chromatin regulatory enzymes that acetylate the positivelycharged lysine tails of nucleosomal histones. This process serves to decondense higher order chromatin structurewhich in turn, activates gene expression. Although it has been established that the misregulation of HATs results indeleterious developmental defects, the mechanism underlying their regulation during development remains unclear.We have previously demonstrated that two human HAT homologs in Drosophila, dmELP3 and dmTIP60, aredifferentially expressed during Drosophila development, suggesting that HAT activity is controlled, at least in part,by regulation of their expression during development. To extend these studies, we are currently using an in situhybridization technique to delineate the tissue and cell type specific expression patterns of these HATs. Ourpreliminary results demonstrate that both dmELP3 and dmTIP60 HATs are also differentially expressed in specifictissues and cell types during various stages of development, suggesting that HAT activity is also controlled at thelevel of tissue and cell-type specific HAT expression profiles.

913CFunctional characterization of the histone acetyltransferase Elp3 during development. Neetu Singh, Felice Elefant.Dept Bioscience/Biotechnology, Drexel University, Philadelphia, PA.

Histone acetyltransferases (HATs) are a class of enzymes that modify chromatin packaging to facilitate geneexpression; however their role during development remains unclear. We are focusing our studies on the DrosophilaHAT (dmHAT) homolog Elp3, as it demonstrates high homology to human Elp3, which plays an essential role intranscriptional activation and elongation, and contains a putative demethylase domain. We first identified dmElp3through database searches and subsequently cloned the cDNA encoding this gene. Alignments between thedmElp3 and human Elp3 proteins demonstrate significant homology: 82% identity, 92% similarity, supporting theuse of this homolog in deciphering human Elp3 developmental function. To characterize dmElp3 function, we areusing an inducible GAL4/RNAi based system in Drosophila to silence endogenous dmELP3 expression in a varietyof tissues and developmental stages. A 650bp non-conserved fragment from dmELP3 was cloned into a sense-antisense inverted gene arrangement under the control of UAS binding sites to induce R

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