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dc.contributor.authorRussell, Brandon S
dc.contributor.authorDedon, Peter C
dc.date.accessioned2020-03-30T11:59:23Z
dc.date.available2020-03-30T11:59:23Z
dc.date.issued2019-06
dc.identifier.issn2375-2548
dc.identifier.urihttps://hdl.handle.net/1721.1/124401
dc.description.abstractNutrient availability has a profound impact on cell fate. Upon nitrogen starvation, wild-type fission yeast cells uncouple cell growth from cell division to generate small, round-shaped cells that are competent for sexual differentiation. The TORC1 (TOR complex 1) and TORC2 complexes exert opposite controls on cell growth and cell differentiation, but little is known about how their activity is coordinated. We show that transfer RNA (tRNA) modifications by Elongator are critical for this regulation by promoting the translation of both key components of TORC2 and repressors of TORC1. We further identified the TORC2 pathway as an activator of Elongator by down-regulating a Gsk3 (glycogen synthase kinase 3)–dependent inhibitory phosphorylation of Elongator. Therefore, a feedback control is operating between TOR complex (TORC) signaling and tRNA modification by Elongator to enforce the advancement of mitosis that precedes cell differentiation.en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (grant ES026856)en_US
dc.language.isoen
dc.publisherAmerican Association for the Advancement of Science (AAAS)en_US
dc.relation.isversionof10.1126/sciadv.aav0184en_US
dc.rightsCreative Commons Attribution NonCommercial License 4.0en_US
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/en_US
dc.sourceScience Advancesen_US
dc.titleReciprocal regulation of TORC signaling and tRNA modifications by Elongator enforces nutrient-dependent cell fateen_US
dc.typeArticleen_US
dc.identifier.citationCandiracci, Julie et al. "Reciprocal regulation of TORC signaling and tRNA modifications by Elongator enforces nutrient-dependent cell fate." Science advances 5(2019): eaav0184 © 2019 The Author(s)en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biological Engineeringen_US
dc.relation.journalScience advancesen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dc.date.updated2020-02-14T18:17:39Z
dspace.date.submission2020-02-14T18:18:00Z
mit.journal.volume5en_US
mit.journal.issue6en_US
mit.licensePUBLISHER_CC


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