PDHK-2 Deficiency Is Associated with Attenuation of Lipase-Mediated Fat Consumption for the Increased Survival of Caenorhabditis elegans Dauers 英文参考文献.docVIP

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PDHK-2 Deficiency Is Associated with Attenuation of Lipase-Mediated Fat Consumption for the Increased Survival of Caenorhabditis elegans Dauers 英文参考文献.doc

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PDHK-2 Deficiency Is Associated with Attenuation of Lipase-Mediated Fat Consumption for the Increased Survival of Caenorhabditis elegans Dauers 英文参考文献

PDHK-2DeficiencyIsAssociatedwithAttenuationof Lipase-MediatedFatConsumptionfortheIncreased SurvivalofCaenorhabditiselegansDauers SunheeKim,E-JinShin,Jeong-HoonHahm,Pil-JongPark,Ji-EunHwang,Young-KiPaik* DepartmentofBiochemistryandIntegratedOmicsforBiomedicalScience,WorldClassUniversityProgram,CollegeofLifeScienceandBiotechnology,YonseiProteome ResearchCenter,YonseiUniversity,Seoul,Korea Abstract In Caenorhabditis elegans, slow fat consumption has been suggested to contribute to the extension of the survival rate duringnutritionallyadverseconditions.Here,weinvestigatedthepotentialroleofpyruvatedehydrogenasekinase(PDHK)- 2, the C. elegans homolog of mammalian PDK, effects on fat metabolism under nutritional conditions. PDHK-2 was expressed at low levels under well-fed conditions but was highly induced during long-term starvation and in the dauer state.Thisincreaseinpdhk-2expressionwasregulatedbybothDAF-16andNHR-49.Dauer-specificinductionofPDHK-2was abolisheduponentryintothepost-dauerstage.Interestingly,inthelong-termdauerstate,storedfatlevelswerehigherin daf-2(e1370);pdhk-2doublemutantsthanindaf-2(e1370),suggestingapositiverelationshipbetweenPDHK-2activityandfat consumption.PDHK-2deficiencyhasbeenshowntoleadtogreaterpreservationofresidualfats,whichwouldbepredicted tocontributetosurvivalduringthedauerstate.Atestofthispredictionshowedthatthesurvivalratesofdaf-2(e1370);pdhk- 2(tm3075)anddaf-2(e1370);pdhk-2(tm3086)doublemutantswerehigherthanthatofdaf-2(e1370),suggestingthatlossof eithertheATP-bindingdomain(tm3075)orbranchedchainketo-aciddehydrogenasekinasedomain(tm3086)ofPDHK-2 leadstoreducedfatconsumptionandthusfavorsincreaseddauersurvival.Thisattenuatedfatconsumptioninthelong- termdauerstateofC.elegansdaf-2(e1370);pdhk-2mutantswasassociatedwithconcomitantdown-regulationofthelipases ATGL (adipose triglyceride lipase), HSL (hormone-sensitive lipase), and C07E3.9 (phospholipase). In contrast, PDHK-2 overexpressioninwild-typestarvedwormsinducedlipaseexpressionandpromoteda