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Nitrogendepedent regulation of Rtg1 and Rtg3 in TOR pathway
Manykeysignalingmoleculesareconservedfromyeasttoman.mTORisaproteinkinaseinvolvedinnutrientandgrowthfactorsignalinginhumansthathasayeasthomologwithasimilarrole,TOR1.Likeitshumancounterpart,yeastTOR1isalsoinhibitedbyrapamycin.SignalingdownstreamoftheTORkinasepathwaysregulatesthenuclearlocalizationofseveraltranscriptionfactorsinresponsetothecarbonandnitrogensourcesinthenutritionalenvironment.YeastcellsactivatethetranscriptionfactorGLN3throughtheTORpathwaytocontroltheuseofnitrogeninresponsetonitrogensensing.TORphosphorylationofGLN3whennitrogenisabundantcausescytoplasmiclocalizationandinactivationofthistranscriptionfactor.Whennitrogenisabundant,URE2alsointeractswithGLN3tokeepitoutofthenucleusandrepressed.TORalsoregulatesGLN3throughregulationofthephosphataseSIT4thatdephosphorylatesGLN3inducingnuclearlocalization.Thepreferrednitrogensourcesforyeastcellsareglutamineandglutamate,whicharederivedfromTCAcycleintermediates.TheuseofureaorammoniaasanitrogensourceisassociatedwithinductionofgenesinvolvedintheTCAcyclebythetranscriptionfactorsRTG1andRTG3.Whenglutamineispresent,itcausesrepressionofRTG1andRTG3byTOR1.ThesetofgenesregulateddownstreamofTORaffectcellgrowthassociatedprocessessuchastranslationandnutrientuse.TheABIlityofTORtoselectivelyregulatedifferentsetsofgenesinresponsetoeithercarbonornitrogensourcesindicatesthatTORcaninteractindependentlywiththesedownstreameffectors.
Contributor:
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