The microprotein Nrs1 rewires the G1/S transcriptional machinery during nitrogen limitation in budding yeast.


Journal

PLoS biology
ISSN: 1545-7885
Titre abrégé: PLoS Biol
Pays: United States
ID NLM: 101183755

Informations de publication

Date de publication:
03 2022
Historique:
received: 21 12 2020
accepted: 19 01 2022
entrez: 3 3 2022
pubmed: 4 3 2022
medline: 22 3 2022
Statut: epublish

Résumé

Commitment to cell division at the end of G1 phase, termed Start in the budding yeast Saccharomyces cerevisiae, is strongly influenced by nutrient availability. To identify new dominant activators of Start that might operate under different nutrient conditions, we screened a genome-wide ORF overexpression library for genes that bypass a Start arrest caused by absence of the G1 cyclin Cln3 and the transcriptional activator Bck2. We recovered a hypothetical gene YLR053c, renamed NRS1 for Nitrogen-Responsive Start regulator 1, which encodes a poorly characterized 108 amino acid microprotein. Endogenous Nrs1 was nuclear-localized, restricted to poor nitrogen conditions, induced upon TORC1 inhibition, and cell cycle-regulated with a peak at Start. NRS1 interacted genetically with SWI4 and SWI6, which encode subunits of the main G1/S transcription factor complex SBF. Correspondingly, Nrs1 physically interacted with Swi4 and Swi6 and was localized to G1/S promoter DNA. Nrs1 exhibited inherent transactivation activity, and fusion of Nrs1 to the SBF inhibitor Whi5 was sufficient to suppress other Start defects. Nrs1 appears to be a recently evolved microprotein that rewires the G1/S transcriptional machinery under poor nitrogen conditions.

Identifiants

pubmed: 35239649
doi: 10.1371/journal.pbio.3001548
pii: PBIOLOGY-D-20-03681
pmc: PMC8893695
doi:

Substances chimiques

DNA-Binding Proteins 0
Repressor Proteins 0
SWI4 protein, S cerevisiae 0
SWI6 protein, S cerevisiae 0
Saccharomyces cerevisiae Proteins 0
Transcription Factors 0
Whi5 protein, S cerevisiae 0
Nitrogen N762921K75

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

e3001548

Subventions

Organisme : NIH HHS
ID : R01 OD010929
Pays : United States
Organisme : CIHR
ID : FDN-167277
Pays : Canada

Commentaires et corrections

Type : ErratumIn

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Sylvain Tollis (S)

Institute of Biomedicine, University of Eastern Finland, Kuopio, Finland.
Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

Jaspal Singh (J)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.

Roger Palou (R)

Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

Yogitha Thattikota (Y)

Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

Ghada Ghazal (G)

Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

Jasmin Coulombe-Huntington (J)

Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

Xiaojing Tang (X)

Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada.

Susan Moore (S)

Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

Deborah Blake (D)

Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

Eric Bonneil (E)

Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

Catherine A Royer (CA)

Department of Biological Sciences, Rensselaer Polytechnic Institute, Troy, New York, United States of America.

Pierre Thibault (P)

Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

Mike Tyers (M)

Institute for Research in Immunology and Cancer, University of Montréal, Montréal, Québec, Canada.

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