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p53 Controls Meiotic Prophase Progression and Crossover Formation

Meiosis initiates with the formation of double strand breaks (DSBs) throughout the genome. To avoid genomic instability, these DSBs need to be correctly repaired by homologous recombination. Surveillance mechanisms involving the DNA damage response (DDR) pathway ATM-CHK2-p53 can detect the persisten...

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Autores principales: Marcet-Ortega, Marina, Maldonado-Linares, Andros, López-Panadés, Maria, Roig, Ignasi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9456223/
https://www.ncbi.nlm.nih.gov/pubmed/36077210
http://dx.doi.org/10.3390/ijms23179818
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author Marcet-Ortega, Marina
Maldonado-Linares, Andros
López-Panadés, Maria
Roig, Ignasi
author_facet Marcet-Ortega, Marina
Maldonado-Linares, Andros
López-Panadés, Maria
Roig, Ignasi
author_sort Marcet-Ortega, Marina
collection PubMed
description Meiosis initiates with the formation of double strand breaks (DSBs) throughout the genome. To avoid genomic instability, these DSBs need to be correctly repaired by homologous recombination. Surveillance mechanisms involving the DNA damage response (DDR) pathway ATM-CHK2-p53 can detect the persistence of unrepaired DBSs and activate the recombination-dependent arrest at the pachytene stage. However, a complete understanding of p53 functions under normal physiological conditions remains lacking. Here, we report a detailed analysis of the p53 role during meiotic prophase in mice spermatocytes. We show that the absence of p53 regulates prophase progression by slowing down the pachytene stage when the recombination-dependent arrest occurs. Furthermore, our results show that p53 is necessary for proper crossover (CO) formation and localization. Our study contributes to a deeper understanding of p53 roles during the meiotic prophase.
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spelling pubmed-94562232022-09-09 p53 Controls Meiotic Prophase Progression and Crossover Formation Marcet-Ortega, Marina Maldonado-Linares, Andros López-Panadés, Maria Roig, Ignasi Int J Mol Sci Article Meiosis initiates with the formation of double strand breaks (DSBs) throughout the genome. To avoid genomic instability, these DSBs need to be correctly repaired by homologous recombination. Surveillance mechanisms involving the DNA damage response (DDR) pathway ATM-CHK2-p53 can detect the persistence of unrepaired DBSs and activate the recombination-dependent arrest at the pachytene stage. However, a complete understanding of p53 functions under normal physiological conditions remains lacking. Here, we report a detailed analysis of the p53 role during meiotic prophase in mice spermatocytes. We show that the absence of p53 regulates prophase progression by slowing down the pachytene stage when the recombination-dependent arrest occurs. Furthermore, our results show that p53 is necessary for proper crossover (CO) formation and localization. Our study contributes to a deeper understanding of p53 roles during the meiotic prophase. MDPI 2022-08-29 /pmc/articles/PMC9456223/ /pubmed/36077210 http://dx.doi.org/10.3390/ijms23179818 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Marcet-Ortega, Marina
Maldonado-Linares, Andros
López-Panadés, Maria
Roig, Ignasi
p53 Controls Meiotic Prophase Progression and Crossover Formation
title p53 Controls Meiotic Prophase Progression and Crossover Formation
title_full p53 Controls Meiotic Prophase Progression and Crossover Formation
title_fullStr p53 Controls Meiotic Prophase Progression and Crossover Formation
title_full_unstemmed p53 Controls Meiotic Prophase Progression and Crossover Formation
title_short p53 Controls Meiotic Prophase Progression and Crossover Formation
title_sort p53 controls meiotic prophase progression and crossover formation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9456223/
https://www.ncbi.nlm.nih.gov/pubmed/36077210
http://dx.doi.org/10.3390/ijms23179818
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