Cargando…

The S. cerevisiae m(6)A-reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts

N(6)-Methyladenosine (m(6)A), one of the most abundant internal modification of eukaryotic mRNAs, participates in the post-transcriptional control of gene expression through recruitment of specific m(6)A readers. In Saccharomyces cerevisiae, the m(6)A methyltransferase Ime4 is expressed only during...

Descripción completa

Detalles Bibliográficos
Autores principales: Scutenaire, Jérémy, Plassard, Damien, Matelot, Mélody, Villa, Tommaso, Zumsteg, Julie, Libri, Domenico, Séraphin, Bertrand
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9881176/
https://www.ncbi.nlm.nih.gov/pubmed/35934316
http://dx.doi.org/10.1093/nar/gkac640
_version_ 1784879058497044480
author Scutenaire, Jérémy
Plassard, Damien
Matelot, Mélody
Villa, Tommaso
Zumsteg, Julie
Libri, Domenico
Séraphin, Bertrand
author_facet Scutenaire, Jérémy
Plassard, Damien
Matelot, Mélody
Villa, Tommaso
Zumsteg, Julie
Libri, Domenico
Séraphin, Bertrand
author_sort Scutenaire, Jérémy
collection PubMed
description N(6)-Methyladenosine (m(6)A), one of the most abundant internal modification of eukaryotic mRNAs, participates in the post-transcriptional control of gene expression through recruitment of specific m(6)A readers. In Saccharomyces cerevisiae, the m(6)A methyltransferase Ime4 is expressed only during meiosis and its deletion impairs this process. To elucidate how m(6)A control gene expression, we investigated the function of the budding yeast m(6)A reader Pho92. We show that Pho92 is an early meiotic factor that promotes timely meiotic progression. High-throughput RNA sequencing and mapping of Pho92-binding sites following UV-crosslinking reveal that Pho92 is recruited to specific mRNAs in an m(6)A-dependent manner during the meiotic prophase, preceding their down-regulation. Strikingly, point mutations altering m(6)A sites in mRNAs targeted by Pho92 are sufficient to delay their down-regulation and, in one case, to slow down meiotic progression. Altogether, our results indicate that Pho92 facilitate the meiotic progression by accelerating the down-regulation of timely-regulated mRNAs during meiotic recombination.
format Online
Article
Text
id pubmed-9881176
institution National Center for Biotechnology Information
language English
publishDate 2022
publisher Oxford University Press
record_format MEDLINE/PubMed
spelling pubmed-98811762023-01-31 The S. cerevisiae m(6)A-reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts Scutenaire, Jérémy Plassard, Damien Matelot, Mélody Villa, Tommaso Zumsteg, Julie Libri, Domenico Séraphin, Bertrand Nucleic Acids Res NAR Breakthrough Article N(6)-Methyladenosine (m(6)A), one of the most abundant internal modification of eukaryotic mRNAs, participates in the post-transcriptional control of gene expression through recruitment of specific m(6)A readers. In Saccharomyces cerevisiae, the m(6)A methyltransferase Ime4 is expressed only during meiosis and its deletion impairs this process. To elucidate how m(6)A control gene expression, we investigated the function of the budding yeast m(6)A reader Pho92. We show that Pho92 is an early meiotic factor that promotes timely meiotic progression. High-throughput RNA sequencing and mapping of Pho92-binding sites following UV-crosslinking reveal that Pho92 is recruited to specific mRNAs in an m(6)A-dependent manner during the meiotic prophase, preceding their down-regulation. Strikingly, point mutations altering m(6)A sites in mRNAs targeted by Pho92 are sufficient to delay their down-regulation and, in one case, to slow down meiotic progression. Altogether, our results indicate that Pho92 facilitate the meiotic progression by accelerating the down-regulation of timely-regulated mRNAs during meiotic recombination. Oxford University Press 2022-08-08 /pmc/articles/PMC9881176/ /pubmed/35934316 http://dx.doi.org/10.1093/nar/gkac640 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of Nucleic Acids Research. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
spellingShingle NAR Breakthrough Article
Scutenaire, Jérémy
Plassard, Damien
Matelot, Mélody
Villa, Tommaso
Zumsteg, Julie
Libri, Domenico
Séraphin, Bertrand
The S. cerevisiae m(6)A-reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts
title The S. cerevisiae m(6)A-reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts
title_full The S. cerevisiae m(6)A-reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts
title_fullStr The S. cerevisiae m(6)A-reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts
title_full_unstemmed The S. cerevisiae m(6)A-reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts
title_short The S. cerevisiae m(6)A-reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts
title_sort s. cerevisiae m(6)a-reader pho92 promotes timely meiotic recombination by controlling key methylated transcripts
topic NAR Breakthrough Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9881176/
https://www.ncbi.nlm.nih.gov/pubmed/35934316
http://dx.doi.org/10.1093/nar/gkac640
work_keys_str_mv AT scutenairejeremy thescerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT plassarddamien thescerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT matelotmelody thescerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT villatommaso thescerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT zumstegjulie thescerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT libridomenico thescerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT seraphinbertrand thescerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT scutenairejeremy scerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT plassarddamien scerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT matelotmelody scerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT villatommaso scerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT zumstegjulie scerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT libridomenico scerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts
AT seraphinbertrand scerevisiaem6areaderpho92promotestimelymeioticrecombinationbycontrollingkeymethylatedtranscripts