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Maternal Oct-4 is a potential key regulator of the developmental competence of mouse oocytes

BACKGROUND: The maternal contribution of transcripts and proteins supplied to the zygote is crucial for the progression from a gametic to an embryonic control of preimplantation development. Here we compared the transcriptional profiles of two types of mouse MII oocytes, one which is developmentally...

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Autores principales: Zuccotti, Maurizio, Merico, Valeria, Sacchi, Lucia, Bellone, Michele, Brink, Thore C, Bellazzi, Riccardo, Stefanelli, Mario, Redi, Carlo Alberto, Garagna, Silvia, Adjaye, James
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576189/
https://www.ncbi.nlm.nih.gov/pubmed/18837968
http://dx.doi.org/10.1186/1471-213X-8-97
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author Zuccotti, Maurizio
Merico, Valeria
Sacchi, Lucia
Bellone, Michele
Brink, Thore C
Bellazzi, Riccardo
Stefanelli, Mario
Redi, Carlo Alberto
Garagna, Silvia
Adjaye, James
author_facet Zuccotti, Maurizio
Merico, Valeria
Sacchi, Lucia
Bellone, Michele
Brink, Thore C
Bellazzi, Riccardo
Stefanelli, Mario
Redi, Carlo Alberto
Garagna, Silvia
Adjaye, James
author_sort Zuccotti, Maurizio
collection PubMed
description BACKGROUND: The maternal contribution of transcripts and proteins supplied to the zygote is crucial for the progression from a gametic to an embryonic control of preimplantation development. Here we compared the transcriptional profiles of two types of mouse MII oocytes, one which is developmentally competent (MII(SN )oocyte), the other that ceases development at the 2-cell stage (MII(NSN )oocyte), with the aim of identifying genes and gene expression networks whose misregulated expression would contribute to a reduced developmental competence. RESULTS: We report that: 1) the transcription factor Oct-4 is absent in MII(NSN )oocytes, accounting for 2) the down-regulation of Stella, a maternal-effect factor required for the oocyte-to-embryo transition and of which Oct-4 is a positive regulator; 3) eighteen Oct-4-regulated genes are up-regulated in MII(NSN )oocytes and are part of gene expression networks implicated in the activation of adverse biochemical pathways such as oxidative phosphorylation, mitochondrial dysfunction and apoptosis. CONCLUSION: The down-regulation of Oct-4 plays a crucial function in a sequence of molecular processes that leads to the developmental arrest of MII(NSN )oocytes. The use of a model study in which the MII oocyte ceases development consistently at the 2-cell stage has allowed to attribute a role to the maternal Oct-4 that has never been described before. Oct-4 emerges as a key regulator of the molecular events that govern the establishment of the developmental competence of mouse oocytes.
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spelling pubmed-25761892008-10-31 Maternal Oct-4 is a potential key regulator of the developmental competence of mouse oocytes Zuccotti, Maurizio Merico, Valeria Sacchi, Lucia Bellone, Michele Brink, Thore C Bellazzi, Riccardo Stefanelli, Mario Redi, Carlo Alberto Garagna, Silvia Adjaye, James BMC Dev Biol Research Article BACKGROUND: The maternal contribution of transcripts and proteins supplied to the zygote is crucial for the progression from a gametic to an embryonic control of preimplantation development. Here we compared the transcriptional profiles of two types of mouse MII oocytes, one which is developmentally competent (MII(SN )oocyte), the other that ceases development at the 2-cell stage (MII(NSN )oocyte), with the aim of identifying genes and gene expression networks whose misregulated expression would contribute to a reduced developmental competence. RESULTS: We report that: 1) the transcription factor Oct-4 is absent in MII(NSN )oocytes, accounting for 2) the down-regulation of Stella, a maternal-effect factor required for the oocyte-to-embryo transition and of which Oct-4 is a positive regulator; 3) eighteen Oct-4-regulated genes are up-regulated in MII(NSN )oocytes and are part of gene expression networks implicated in the activation of adverse biochemical pathways such as oxidative phosphorylation, mitochondrial dysfunction and apoptosis. CONCLUSION: The down-regulation of Oct-4 plays a crucial function in a sequence of molecular processes that leads to the developmental arrest of MII(NSN )oocytes. The use of a model study in which the MII oocyte ceases development consistently at the 2-cell stage has allowed to attribute a role to the maternal Oct-4 that has never been described before. Oct-4 emerges as a key regulator of the molecular events that govern the establishment of the developmental competence of mouse oocytes. BioMed Central 2008-10-06 /pmc/articles/PMC2576189/ /pubmed/18837968 http://dx.doi.org/10.1186/1471-213X-8-97 Text en Copyright © 2008 Zuccotti et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Zuccotti, Maurizio
Merico, Valeria
Sacchi, Lucia
Bellone, Michele
Brink, Thore C
Bellazzi, Riccardo
Stefanelli, Mario
Redi, Carlo Alberto
Garagna, Silvia
Adjaye, James
Maternal Oct-4 is a potential key regulator of the developmental competence of mouse oocytes
title Maternal Oct-4 is a potential key regulator of the developmental competence of mouse oocytes
title_full Maternal Oct-4 is a potential key regulator of the developmental competence of mouse oocytes
title_fullStr Maternal Oct-4 is a potential key regulator of the developmental competence of mouse oocytes
title_full_unstemmed Maternal Oct-4 is a potential key regulator of the developmental competence of mouse oocytes
title_short Maternal Oct-4 is a potential key regulator of the developmental competence of mouse oocytes
title_sort maternal oct-4 is a potential key regulator of the developmental competence of mouse oocytes
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576189/
https://www.ncbi.nlm.nih.gov/pubmed/18837968
http://dx.doi.org/10.1186/1471-213X-8-97
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