Steroid Regulation of Midgut Cell Death during Drosophila Development

Developmental Biology

Cheng-Yu Lee¹  Bridget A.K. Cooksey¹  Eric H. Baehrecke¹ 

[1] Center for Biosystems Research, University of Maryland Biotechnology Institute, University of Maryland, College Park, Maryland, 20742

关键词: steroid;    ecdysone;    programmed cell death;    apoptosis;    autophagy;    development;    metamorphosis;    Drosophila;   

DOI  :  10.1006/dbio.2002.0784

学科分类：生物科学（综合）

来源: Academic Press

【 摘 要 】

Steroidhormonestriggerdynamictissuechangesduringanimaldevelopmentbyactivatingcellproliferation,celldifferentiation,andcelldeath.HerewecharacterizesteroidregulationofchangesinmidgutstructureduringtheonsetofDrosophilametamorphosis.Followinganincreaseinthesteroid20-hydroxyecdysone(ecdysone)attheendoflarvaldevelopment,futureadultmidgutepitheliumisformed,andthelarvalmidgutisrapidlydestroyed.Mutationsinthesteroid-regulatedgenesBR-CandE93differentiallyimpactlarvalmidgutcelldeathbutdonotaffecttheformationofadultmidgutepithelia.Incontrast,mutationsintheecdysone-regulatedE74AandE74Bgenesdonotappeartoperturbmidgutdevelopmentduringmetamorphosis.Larvalmidgutcellspossessvacuolesthatcontaincellularorganelles,indicatingthatthesecellsdiebyautophagy.WhilemutationsintheBR-C,E74,andE93genesdonotimpactDNAdegradationduringthiscelldeath,mutationsinBR-Cinhibitdestructionoflarvalmidgutstructures,includingtheproventriculusandgastriccaeca,andE93mutantsexhibitdecreasedformationofautophagicvacuoles.Dyingmidgutsexpresstherpr,hid,ark,dronc,andcrqcelldeathgenes,suggestingthatthecorecelldeathmachineryisinvolvedinlarvalmidgutcelldeath.Thetranscriptionofrpr,hid,andcrqarealteredinBR-Cmutants,andE93mutantspossessalteredtranscriptionofthecaspasedronc,providingamechanismforthedisruptionofmidgutcelldeathinthesemutantanimals.Thesestudiesindicatethatecdysonetriggersatwo-stephierarchycomposedofsteroid-inducedregulatorygenesandapoptosisgenesthat,inturn,regulatetheautophagicdeathofmidgutcellsduringdevelopment.

【 授权许可】

Unknown