An experimental analysis of the pigment defect caused by mutations at the W and Sl loci in mice☆☆☆

[摘要] ThepigmentdefectcausedbymutationsattheWandSllociinmicewasinvestigatedbygraftingnormalandmutantembryonicskinandneuralcrestinvariouscombinationstothecoelomofhostchickembryos.Sincethemutanthomozygotesofbothlociaresterile,embryoswereproducedbybreedingheterozygotesandthereforeonlyone-fourthoftheresultingembryoswereexpectedtobeoftheblack-eyedwhitephenotype.GraftsobtainedfromthecombinationofSlneuraltubeswith+/+skinproducedpigmentinallthecasesrecovered.Thereciprocalcombinationof+/+neuraltubeswithSlskinfailedtoproducepigmentinthegraftedskinin33%ofthecases.Ontheotherhand,graftsproducedbycombining+/+tubeswithWskinresultedin100%pigmentproduction,whereasonly39%oftheWtube-+/+skincombinationgraftsformedpigment.Theseresultsindicatedthattheblack-eyedwhitephenotypeinSlandWhomozygoteswascausedbygeneactionatdifferentsites.IntheWmutants,theneuralcrestappearedtobeabnormal,andintheSlmutants,theskinwasinvolved.Astudyofthepigmentoccurrencein4nonepidermallocationsof5dayWandSlmicerevealedthatageneralpigmentreductionintheselocationsresultedfromtheactionofbothmutantgenes.SinceinthecaseofSlthepigment-formingcomponentoftheneuralcrestwasfoundtobenormal,itappearedthattheskinaffectedthedifferentiationofnonepidermalmelanoblastsaswellasthoseintheskin.Alternatively,othertissuesinadditiontotheskinmightbeaffectedbySlandtherebyresultinthegeneralpigmentcellreduction.Therelationshipbetweenthepigmentdefect,macrocyticanemiaanddeficiencyofprimordialgermcellsproducedbythetwomutantgenesremainsobscure.ItisnoteworthythatboththepigmentdefectandtheanemiaintheWmutantsaretheresultsoffactorsactingwithinthepigmentandbloodformingcellsthemselves.InthecaseofSl,thetissueenvironmentsinwhichthemelanoblastsandhematopoieticcellsresideareresponsibleforproducingthetwoabnormalities.

[学科分类] 生物科学（综合）