ABSTRACT
Durstonandcolleagues(85)treatedXenopusembryoswithw-5-10-6MRA betweenlateblastulaandearlyneurulastagesandobservedthattheresulting embryosfailedtodevelopanteriorneuralstructures(forebrain,midbrain,eyes). Identicaleffectsareseenwithaxolotlembryos(86).Sincethetotalvolumeof CNStissue,estimatedfromsectionsofRA-treatedembryos,wasthesameasin controls,Durstonetal.(85)concludedthatthemissinganteriorneuralstructures hadbeenrespecifiedtoformposteriorneuralstructures.Thiswasanexciting conclusionbecauseposteriorizationofthemesodermispreciselywhatRAdoes inthelimb(seeabove)anduniversalityofeffectsisacontinualdesireof embryologists.Theseanatomicdeficienciesalsoreflectalterationsingene activity,asitwasshownthatanterior-specificgenessuchasXCG-1,XAG-1, XA-1,andengrailedarerepressedwhereastheactivityofXJF-3andaposterior geneXlHbox6isincreased(87,88).Furtherexperimentshaveconfirmedthatone ofthetargetsofRAadministrationtotheembryoistheneuralectoderm(88-92) andprovidedanevengreaterparalleltothelimbbudbyallowingfortheinterpretationthattheremaybeanendogenousgradientofRAwithintheneuralplate withahighpointattheposteriorend(92).IntheseexperimentsRAwasshownto mimicnormaldevelopmentbygeneratingthecorrectspatialpatternofexpression oftwogenes,X1Hbox6andXIF6,inisolatedexplantsofXenopusanimalcaps. Theproposedposteriortransformationwouldthereforecomeaboutbecauseofthe elevationofthisgradientbytheadministrationofexcessRA.
