A gain-of-function mutation in oma-1, a C. elegans gene required for oocyte maturation, results in delayed degradation of maternal proteins and embryonic lethality

摘要

Invertebrates,oocytesundergomaturation,arrestinmetaphaseII,andcanthenbefertilizedbysperm.Fertilizationinitiatesmoleculareventsthatleadtotheactivationofearlyembryonicdevelopment.InemCaenorhabditiselegans,/emwherenodelaybetweenoocytematurationandfertilizationisapparent,oocytematurationandfertilizationmustbetightlycoordinated.ItisnotclearwhatcoordinatesthetransitionfromanoocytetoanembryoinemC.elegans,/embutregulatedturnoverofoocyte-specificproteinscontributestotheprocess.Wedescribehereagain-of-functionmutation(emzu405/em)inagenethatisessentialforoocytematuration,emoma-1./emInwildtypeanimals,OMA-1proteinisexpressedatahighlevelexclusivelyinoocytesandnewlyfertilizedembryosandisdegradedrapidlyafterthefirstmitoticdivision.Theemzu405/emmutationresultsinimproperdegradationoftheOMA-1proteininembryos.Inemoma-1(zu405)/emembryos,theCblastomereistransformedtotheEMSblastomerefate,resultinginembryoniclethality.Weshowthatdegradationofseveralmaternallysuppliedcellfatedeterminants,includingSKN-1,PIE-1,MEX-3,andMEX-5,isdelayedinemoma-1(zu405)/emmutantembryos.Inwildtypeembryos,SKN-1functionsinEMSforEMSblastomerefatespecification.AdecreasedlevelofmaternalSKN-1proteinintheCblastomererelativetoEMSisbelievedtoberesponsibleforthiscellexpressingtheC,insteadoftheEMS,fate.DelayeddegradationofmaternalSKN-1proteininemoma-1(zu405)/emembryosandresultantelevatedlevelsinCblastomereislikelyresponsiblefortheobservedC-to-EMSblastomerefatetransformation.Theseobservationssuggestthatemoma-1,/eminadditiontoitsroleinoocytematuration,contributestoearlyembryonicdevelopmentbyregulatingthetemporaldegradationofmaternalproteinsinearlyemC.elegans/emembryos./p/div