CNOT6/6L-mediated mRNA degradation in ovarian granulosa cells is a key mechanism of gonadotropin-triggered follicle development

Summary: CCR4-NOT deadenylase is a major regulator of mRNA turnover. It contains two heterogeneous catalytic subunits CNOT7/8 and CNOT6/6L in vertebrates. The physiological function of each catalytic subunit is unclear due to the gene redundancy. In this study, Cnot6/6l double knockout mice are gene...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Xing-Xing Dai, Zhi-Yan Jiang, Yun-Wen Wu, Qian-Qian Sha, Yang Liu, Jia-Yi Ding, Wen-Dong Xi, Jing Li, Heng-Yu Fan
Formato: article
Lenguaje:EN
Publicado: Elsevier 2021
Materias:
Acceso en línea:https://doaj.org/article/7804dcdc6b2041b8839bd5309aa88b29
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:7804dcdc6b2041b8839bd5309aa88b29
record_format dspace
spelling oai:doaj.org-article:7804dcdc6b2041b8839bd5309aa88b292021-11-18T04:47:54ZCNOT6/6L-mediated mRNA degradation in ovarian granulosa cells is a key mechanism of gonadotropin-triggered follicle development2211-124710.1016/j.celrep.2021.110007https://doaj.org/article/7804dcdc6b2041b8839bd5309aa88b292021-11-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2211124721014856https://doaj.org/toc/2211-1247Summary: CCR4-NOT deadenylase is a major regulator of mRNA turnover. It contains two heterogeneous catalytic subunits CNOT7/8 and CNOT6/6L in vertebrates. The physiological function of each catalytic subunit is unclear due to the gene redundancy. In this study, Cnot6/6l double knockout mice are generated. Cnot6l−/− female mice are infertile, with poor ovarian responses to gonadotropins. Follicle-stimulating hormone (FSH) stimulates the transcription and translation of Cnot6 and Cnot6l in ovarian granulosa cells. CNOT6/6L function as key effectors of FSH in granulosa cells and trigger the clearance of specific transcripts in granulosa cells during preantral to antral follicle transition. These results demonstrate that FSH modulates granulosa cell function by stimulating selective translational activation and degradation of existing mRNAs, in addition to inducing de novo gene transcription. Meanwhile, this study provides in vivo evidence that CNOT6/6L-mediated mRNA deadenylation is dispensable in most somatic cell types, but is essential for female reproductive endocrine regulation.Xing-Xing DaiZhi-Yan JiangYun-Wen WuQian-Qian ShaYang LiuJia-Yi DingWen-Dong XiJing LiHeng-Yu FanElsevierarticlefollicle-stimulating hormonemRNA stabilitymRNA translationPI3K signaling pathwayfemale reproductionovulationBiology (General)QH301-705.5ENCell Reports, Vol 37, Iss 7, Pp 110007- (2021)
institution DOAJ
collection DOAJ
language EN
topic follicle-stimulating hormone
mRNA stability
mRNA translation
PI3K signaling pathway
female reproduction
ovulation
Biology (General)
QH301-705.5
spellingShingle follicle-stimulating hormone
mRNA stability
mRNA translation
PI3K signaling pathway
female reproduction
ovulation
Biology (General)
QH301-705.5
Xing-Xing Dai
Zhi-Yan Jiang
Yun-Wen Wu
Qian-Qian Sha
Yang Liu
Jia-Yi Ding
Wen-Dong Xi
Jing Li
Heng-Yu Fan
CNOT6/6L-mediated mRNA degradation in ovarian granulosa cells is a key mechanism of gonadotropin-triggered follicle development
description Summary: CCR4-NOT deadenylase is a major regulator of mRNA turnover. It contains two heterogeneous catalytic subunits CNOT7/8 and CNOT6/6L in vertebrates. The physiological function of each catalytic subunit is unclear due to the gene redundancy. In this study, Cnot6/6l double knockout mice are generated. Cnot6l−/− female mice are infertile, with poor ovarian responses to gonadotropins. Follicle-stimulating hormone (FSH) stimulates the transcription and translation of Cnot6 and Cnot6l in ovarian granulosa cells. CNOT6/6L function as key effectors of FSH in granulosa cells and trigger the clearance of specific transcripts in granulosa cells during preantral to antral follicle transition. These results demonstrate that FSH modulates granulosa cell function by stimulating selective translational activation and degradation of existing mRNAs, in addition to inducing de novo gene transcription. Meanwhile, this study provides in vivo evidence that CNOT6/6L-mediated mRNA deadenylation is dispensable in most somatic cell types, but is essential for female reproductive endocrine regulation.
format article
author Xing-Xing Dai
Zhi-Yan Jiang
Yun-Wen Wu
Qian-Qian Sha
Yang Liu
Jia-Yi Ding
Wen-Dong Xi
Jing Li
Heng-Yu Fan
author_facet Xing-Xing Dai
Zhi-Yan Jiang
Yun-Wen Wu
Qian-Qian Sha
Yang Liu
Jia-Yi Ding
Wen-Dong Xi
Jing Li
Heng-Yu Fan
author_sort Xing-Xing Dai
title CNOT6/6L-mediated mRNA degradation in ovarian granulosa cells is a key mechanism of gonadotropin-triggered follicle development
title_short CNOT6/6L-mediated mRNA degradation in ovarian granulosa cells is a key mechanism of gonadotropin-triggered follicle development
title_full CNOT6/6L-mediated mRNA degradation in ovarian granulosa cells is a key mechanism of gonadotropin-triggered follicle development
title_fullStr CNOT6/6L-mediated mRNA degradation in ovarian granulosa cells is a key mechanism of gonadotropin-triggered follicle development
title_full_unstemmed CNOT6/6L-mediated mRNA degradation in ovarian granulosa cells is a key mechanism of gonadotropin-triggered follicle development
title_sort cnot6/6l-mediated mrna degradation in ovarian granulosa cells is a key mechanism of gonadotropin-triggered follicle development
publisher Elsevier
publishDate 2021
url https://doaj.org/article/7804dcdc6b2041b8839bd5309aa88b29
work_keys_str_mv AT xingxingdai cnot66lmediatedmrnadegradationinovariangranulosacellsisakeymechanismofgonadotropintriggeredfollicledevelopment
AT zhiyanjiang cnot66lmediatedmrnadegradationinovariangranulosacellsisakeymechanismofgonadotropintriggeredfollicledevelopment
AT yunwenwu cnot66lmediatedmrnadegradationinovariangranulosacellsisakeymechanismofgonadotropintriggeredfollicledevelopment
AT qianqiansha cnot66lmediatedmrnadegradationinovariangranulosacellsisakeymechanismofgonadotropintriggeredfollicledevelopment
AT yangliu cnot66lmediatedmrnadegradationinovariangranulosacellsisakeymechanismofgonadotropintriggeredfollicledevelopment
AT jiayiding cnot66lmediatedmrnadegradationinovariangranulosacellsisakeymechanismofgonadotropintriggeredfollicledevelopment
AT wendongxi cnot66lmediatedmrnadegradationinovariangranulosacellsisakeymechanismofgonadotropintriggeredfollicledevelopment
AT jingli cnot66lmediatedmrnadegradationinovariangranulosacellsisakeymechanismofgonadotropintriggeredfollicledevelopment
AT hengyufan cnot66lmediatedmrnadegradationinovariangranulosacellsisakeymechanismofgonadotropintriggeredfollicledevelopment
_version_ 1718425047787372544