TOR inactivation triggers heterochromatin formation in rDNA during glucose starvation.


Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
28 Nov 2023
Historique:
received: 08 05 2023
revised: 29 08 2023
accepted: 05 10 2023
medline: 4 12 2023
pubmed: 2 11 2023
entrez: 1 11 2023
Statut: ppublish

Résumé

In response to environmental cues, such as nutrient starvation, living organisms modulate gene expression through mechanisms involving histone modifications. Specifically, nutrient depletion inactivates the TOR (target of rapamycin) pathway, leading to reduced expression of ribosomal genes. While these regulatory mechanisms are well elucidated in budding yeast Saccharomyces cerevisiae, their conservation across diverse organisms remains unclear. In this study, we demonstrate that fission yeast Schizosaccharomyces pombe cells repress ribosomal gene transcription through a different mechanism. TORC1, which accumulates in the rDNA region, dissociates upon starvation, resulting in enhanced methylation of H3K9 and heterochromatin formation, facilitated by dissociation of the stress-responsive transcription factor Atf1 and accumulation of the histone chaperone FACT. We propose that this mechanism might be adapted in mammals that possess Suv39H1 and HP1, which are absent in budding yeast.

Identifiants

pubmed: 37913773
pii: S2211-1247(23)01332-3
doi: 10.1016/j.celrep.2023.113320
pii:
doi:

Substances chimiques

Schizosaccharomyces pombe Proteins 0
Heterochromatin 0
DNA, Ribosomal 0
Transcription Factors 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

113320

Informations de copyright

Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors declare no competing interests.

Auteurs

Hayato Hirai (H)

Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo 153-8902, Japan. Electronic address: h-hirai@bio.c.u-tokyo.ac.jp.

Yuki Sen (Y)

Department of Integrated Sciences, College of Arts and Sciences, The University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo 153-8902, Japan.

Miki Tamura (M)

Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo 153-8902, Japan.

Kunihiro Ohta (K)

Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo 153-8902, Japan; Universal Biology Institute, The University of Tokyo, Hongo 7-3-1, Bunkyo-ku, Tokyo 113-0033, Japan. Electronic address: kohta-pub2@bio.c.u-tokyo.ac.jp.

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Classifications MeSH