PLR-1, a putative E3 ubiquitin ligase, controls cell polarity and axonal extensions in C. elegans

摘要

Duringembryonicdevelopmentneuronsdifferentiateandextendaxonsanddendritesthathavetoreachtheirappropriatetargets.InemCaenorhabditiselegans/emtheAVGneuronisthefirstneurontoextendanaxonduringtheestablishmentoftheventralnervecord,themajorlongitudinalaxontractintheanimal.Ingeneticscreensweisolatedallelesofemplr-1/em,whichcausedpolarityreversalsoftheAVGneuronaswellasoutgrowthandnavigationdefectsoftheAVGaxon.Inadditionemplr-1/emmutantsshowoutgrowthdefectsinseveralotherclassesofneuronsaswellastheposteriorexcretorycanals.emplr-1/emispredictedtoencodeatransmembraneE3ubiquitinligaseandiswidelyexpressedintheanimalincludingtheAVGneuronandtheexcretorycell.emplr-1/emhasrecentlybeenshowntonegativelyregulateWntsignallingbyremovingWntreceptorsfromthecellsurface.WeobservedthatmutationsinagenereducingWntsignallingaswellasmutationsinemunc-53/em/NAV2andemunc-73/em/TriosuppresstheAVGpolaritydefectsinemplr-1/emmutants,butnotthedefectsseeninothercells.Thisplacesemplr-1/eminaWntregulationpathway,butalsosuggeststhatemplr-1/emhasWntindependentfunctionsandinteractswithemunc-53/emandemunc-73/emtocontrolcellpolarity./p/div