Functional Dissection of Caenorhabditis elegans CLK-2TEL2 Cell Cycle Defects during Embryogenesis and Germline Development 英文参考文献.docVIP

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Functional Dissection of Caenorhabditis elegans CLK-2TEL2 Cell Cycle Defects during Embryogenesis and Germline Development 英文参考文献.doc

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Functional Dissection of Caenorhabditis elegans CLK-2TEL2 Cell Cycle Defects during Embryogenesis and Germline Development 英文参考文献

FunctionalDissectionofCaenorhabditiselegansCLK-2/ TEL2CellCycleDefectsduringEmbryogenesisand GermlineDevelopment SandraC.Moser1,SophievonElsner2,IngoBu¨ssing2¤a,ArnoAlpi1¤b,RalfSchnabel2,AntonGartner1* 1Wellcome Trust Centre for Gene Regulation and Expression, College of Life Sciences, University of Dundee, Dundee, Scotland, United Kingdom, 2Developmental Genetics,TechnischeUniversita¨t Braunschweig,Braunschweig,Germany Abstract CLK-2/TEL2isessentialforviabilityfromyeaststovertebrates,butitsessentialfunctionsremainilldefined.CLK-2/TEL2was initially implicated in telomere length regulation in budding yeast, but work in Caenorhabditis elegans has uncovered a function in DNA damage response signalling. Subsequently, DNA damage signalling defects associated with CLK-2/TEL2 have been confirmed in yeast and human cells. The CLK-2/TEL2 interaction with the ATM and ATR DNA damage sensor kinasesanditsrequirementfortheirstabilityledtotheproposalthatCLK-2/TEL2mutantsmightphenocopyATMand/or ATRdepletion.WeuseC.eleganstodissectdevelopmentalandcellcyclerelatedrolesofCLK-2.Temperaturesensitive(ts) clk-2mutantsaccumulategenomicinstabilityandshowadelayofembryoniccellcycletiming.Thisdelaypartiallydepends on the worm p53 homolog CEP-1 and is rescued by co-depletion of the DNA replication checkpoint proteins ATL-1 (C. elegansATR)andCHK-1.Inaddition,clk-2tsmutantsshowaspindleorientationdefectintheeightcellstagesthatleadto major cell fate transitions. clk-2 deletion worms progress through embryogenesis and larval development by maternal rescuebutbecomesterileandhaltgermcellcycleprogression.UnlikeATL-1depletedgermcells,clk-2–nullgermcellsdo notaccumulateDNAdouble-strandbreaks.Rather,clk-2mutantgermcellsarrestwithduplicatedcentrosomesbutwithout mitoticspindlesinanearlyprophaselikestage.Thisgermcellcyclearrestdoesnotdependoncep-1,theDNAreplication,or the spindle checkpoint. Our analysis shows that CLK-2 depletion does not phenocopy PIKK kinase depletion. Rather, we implicateCLK-2inmultip