Staufen targets coracle mRNA to Drosophila neuromuscular junctions and regulates GluRIIA synaptic accumulation and bouton number

摘要

Thepost-synaptictranslationoflocalisedmRNAshasbeenpostulatedtounderlieseveralformsofplasticityatvertebratesynapses,butthemechanismsthattargetmRNAstothesepostsynapticsitesarenotwellunderstood.HereweshowthattheevolutionaryconserveddsRNAbindingprotein,Staufen,localisestothepostsynapticsideoftheemDrosophila/emneuromuscularjunction(NMJ),whereitisrequiredforthelocalisationofemcoracle/emmRNAandprotein.Staufenplaysawell-characterisedroleinthelocalisationofemoskar/emmRNAtotheoocyteposterior,whereStaufendsRNA-bindingdomain5isspecificallyrequiredforitstranslation.RemovalofStaufendsRNA-bindingdomain5,disruptsthepostsynapticaccumulationofCoracleproteinwithoutaffectingthelocalisationofemcora/emmRNA,suggestingthatStaufensimilarlyregulatesCoracletranslation.TropomyosinII,whichfunctionswithStaufeninemoskar/emmRNAlocalisation,isalsorequiredforemcoracle/emmRNAlocalisation,suggestingthatsimilarmechanismstargetmRNAstotheNMJandtheoocyteposterior.Coracle,theorthologueofvertebrateband4.1,functionsintheanchoringoftheglutamatereceptorIIAsubunit(GluRIIA)atthesynapse.Consistentwiththis,emstaufen/emmutantlarvaeshowreducedaccumulationofGluRIIAatsynapses.TheNMJsofemstaufen/emmutantlarvaehavealsoareducednumberofsynapticboutons.Altogether,thissuggeststhatthisnovelStaufen-dependentmRNAlocalisationandlocaltranslationpathwaymayplayaroleinthedevelopmentallyregulatedgrowthoftheNMJ./p/div