Ubiquitination-dependent control of sexual differentiation in fission yeast

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Abstract

In fission yeast, meiosis-specific transcripts are selectively eliminated during vegetative growth by the combined action of the YTH-family RNA-binding protein Mmi1 and the nuclear exosome. Upon nutritional starvation, the master regulator of meiosis Mei2 inactivates Mmi1, thereby allowing expression of the meiotic program. Here, we show that the E3 ubiquitin ligase subunit Not4/Mot2 of the evolutionarily conserved Ccr4-Not complex, which associates with Mmi1, promotes suppression of meiotic transcripts expression in mitotic cells. Our analyses suggest that Mot2 directs ubiquitination of Mei2 to preserve the activity of Mmi1 during vegetative growth. Importantly, Mot2 is not involved in the constitutive pathway of Mei2 turnover, but rather plays a regulatory role to limit its accumulation or inhibit its function. We propose that Mmi1 recruits the Ccr4-Not complex to counteract its own inhibitor Mei2, thereby locking the system in a stable state that ensures the repression of the meiotic program by Mmi1.

Data availability

The following data sets were generated

(2017) Ubiquitination-dependent control of sexual differentiation in fission yeast
Publicly available at NCBI Gene Expression Omnibus (accession no: GSE72327).

https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE72327

Article and author information

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Fabrizio Simonetti

Institut Jacques Monod, Université Paris-Diderot, Paris, France

Competing interests
The authors declare that no competing interests exist.
Tito Candelli

Institut Jacques Monod, Université Paris-Diderot, Paris, France

Competing interests
The authors declare that no competing interests exist.
Sebastien Leon

Institut Jacques Monod, Université Paris-Diderot, Paris, France

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-2536-8595
Domenico Libri

Institut Jacques Monod, Université Paris-Diderot, Paris, France

Competing interests
The authors declare that no competing interests exist.
Mathieu Rougemaille

Institut de Biologie Intégrative de la Cellule, CNRS, UMR9198, Université Paris-Saclay, Gif-sur-Yvette, France

For correspondence
mathieu.rougemaille@i2bc.paris-saclay.fr

Competing interests
The authors declare that no competing interests exist.

"This ORCID iD identifies the author of this article:" 0000-0002-9675-3888

Funding

Fondation Bettencourt Schueller (prix Coup d'Elan 2009)

Domenico Libri

Fondation ARC pour la Recherche sur le Cancer (Projet Fondation ARC 1782)

Mathieu Rougemaille

Agence Nationale de la Recherche (ANR-2016-CE12-0031-01)

Mathieu Rougemaille

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Copyright

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.