Drosophila melanogaster Acetyl-CoA-Carboxylase Sustains a Fatty Acid–Dependent Remote Signal to Waterproof the Respiratory System 英文参考文献.docVIP

下载本文档

7
0
约7.4万字
约 16页
2017-05-11 发布于上海
举报
版权申诉

Drosophila melanogaster Acetyl-CoA-Carboxylase Sustains a Fatty Acid–Dependent Remote Signal to Waterproof the Respiratory System 英文参考文献.doc

1、本文档共16页，可阅读全部内容。
2、原创力文档（book118）网站文档一经付费（服务费），不意味着购买了该文档的版权，仅供个人/单位学习、研究之用，不得用于商业用途，未经授权，严禁复制、发行、汇编、翻译或者网络传播等，侵权必究。
3、本站所有内容均由合作方或网友上传，本站不对文档的完整性、权威性及其观点立场正确性做任何保证或承诺！文档内容仅供研究参考，付费前请自行鉴别。如您付费，意味着您自己接受本站规则且自行承担风险，本站不退款、不进行额外附加服务；查看《如何避免下载的几个坑》。如果您已付费下载过本站文档，您可以点击这里二次下载。
4、如文档侵犯商业秘密、侵犯著作权、侵犯人身权等，请点击“版权申诉”（推荐），也可以打举报电话：400-050-0827(电话支持时间：9:00-18:30)。
5、该文档为VIP文档，如果想要下载，成为VIP会员后，下载免费。
6、成为VIP后，下载本文档将扣除1次下载权益。下载后，不支持退款、换文档。如有疑问请联系我们。
7、成为VIP后，您将拥有八大权益，权益包括：VIP文档下载权益、阅读免打扰、文档格式转换、高级专利检索、专属身份标志、高级客服、多端互通、版权登记。
8、VIP文档为合作方或网友上传，每下载1次，网站将根据用户上传文档的质量评分、类型等，对文档贡献者给予高额补贴、流量扶持。如果你也想贡献VIP文档。上传文档

Drosophila melanogaster Acetyl-CoA-Carboxylase Sustains a Fatty Acid–Dependent Remote Signal to Waterproof the Respiratory System 英文参考文献

DrosophilamelanogasterAcetyl-CoA-Carboxylase SustainsaFattyAcid–DependentRemoteSignalto WaterprooftheRespiratorySystem Jean-PhilippeParvy1,2.,LauraNapal1,3.¤a,ThomasRubin1,3¤b,MickaelPoidevin1,3,LaurentPerrin4, ClaudeWicker-Thomas5,JacquesMontagne1,3* 1CNRS,CentredeGe′ne′tiqueMole′culaire,UPR3404,Gif-sur-Yvette,France,2Universite′PierreetMarieCurie-Paris6,Paris,France,3Universite′Paris-Sud11,Orsay,France, 4IBDML,Universite′ delaMe′diterrane′e,Marseille,France,5CNRS,LEGS,UPR9034,Gif-sur-Yvette,France Abstract Fattyacid(FA)metabolismplaysacentralroleinbodyhomeostasisandrelateddiseases.Thus,FAmetabolicenzymesare attractivetargetsfordrugtherapy.MousestudiesonAcetyl-coenzymeA-carboxylase(ACC),therate-limitingenzymeforFA synthesis,havehighlighteditshomeostaticroleinliverandadiposetissue.Wetookadvantageofthepowerfulgeneticsof Drosophila melanogaster to investigate the role of the unique Drosophila ACC homologue in the fat body and the oenocytes.Thefatbodyaccomplisheshepaticandstoragefunctions,whereastheoenocytesareproposedtoproducethe cuticularlipidsandtocontributetothehepaticfunction.RNA–interferingdisruptionofACCinthefatbodydoesnotaffect viabilitybutdoesresultinadramaticreductionintriglyceridestorageandaconcurrentincreaseinglycogenaccumulation. Thesemetabolicperturbationsfurtherhighlighttheroleoftriglycerideandglycogenstorageincontrollingcirculatorysugar levels,therebyvalidatingDrosophilaasarelevantmodeltoexplorethetissue-specificfunctionofFAmetabolicenzymes.In contrast,ACCdisruptionintheoenocytesthroughRNA–interferenceortissue-targetedmutationinduceslethality,asdoes oenocyteablation.Surprisingly,thislethalityisassociatedwithafailureinthewatertightnessofthespiracles—theorgans controllingtheentryofairintothetrachea.Atthecellularlevel,wehaveobservedthat,indefectivespiracles,lipidsfailto transferfromthespiracularglandtothepointofairentry.Thisphenotypeiscausedbydisruptedsynthesisofaputative very-long-chain-FA(VLCFA)withintheoenocytes,whichultimatelyresultsinalethalanoxicis