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Article: Disruption of Tsc2 in oocytes leads to overactivation of the entire pool of primordial follicles

TitleDisruption of Tsc2 in oocytes leads to overactivation of the entire pool of primordial follicles
Authors
KeywordsPremature ovarian failure
Oocytes
Follicular activation
Tsc/mTOR signaling
Issue Date2009
Citation
Molecular Human Reproduction, 2009, v. 15, n. 12, p. 765-770 How to Cite?
AbstractTo maintain the length of reproductive life in a woman, it is essential that most of her ovarian primordial follicles are maintained in a quiescent state to provide a continuous supply of oocytes. However, our understanding of the molecular mechanisms that control the quiescence and activation of primordial follicles is still in its infancy. In this study, we provide some genetic evidence to show that the tumor suppressor tuberous sclerosis complex 2 (Tsc2), which negatively regulates mammalian target of rapamycin complex 1 (mTORC1), functions in oocytes to maintain the dormancy of primordial follicles. In mutant mice lacking the Tsc2 gene in oocytes, the pool of primordial follicles is activated prematurely due to elevated mTORC1 activity in oocytes. This results in depletion of follicles in early adulthood, causing premature ovarian failure (POF). Our results suggest that the Tsc1-Tsc2 complex mediated suppression of mTORC1 activity is indispensable for maintenance of the dormancy of primordial follicles, thus preserving the follicular pool, and that mTORC1 activity in oocytes promotes follicular activation. Our results also indicate that deregulation of Tsc/mTOR signaling in oocytes may cause pathological conditions of the ovary such as infertility and POF. © The Author 2009. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.
Persistent Identifierhttp://hdl.handle.net/10722/265411
ISSN
2023 Impact Factor: 3.6
2023 SCImago Journal Rankings: 1.201
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAdhikari, Deepak-
dc.contributor.authorFlohr, Gilian-
dc.contributor.authorGorre, Nagaraju-
dc.contributor.authorShen, Yan-
dc.contributor.authorYang, Hairu-
dc.contributor.authorLundin, Eva-
dc.contributor.authorLan, Zijian-
dc.contributor.authorGambello, Michael J.-
dc.contributor.authorLiu, Kui-
dc.date.accessioned2018-12-03T01:20:34Z-
dc.date.available2018-12-03T01:20:34Z-
dc.date.issued2009-
dc.identifier.citationMolecular Human Reproduction, 2009, v. 15, n. 12, p. 765-770-
dc.identifier.issn1360-9947-
dc.identifier.urihttp://hdl.handle.net/10722/265411-
dc.description.abstractTo maintain the length of reproductive life in a woman, it is essential that most of her ovarian primordial follicles are maintained in a quiescent state to provide a continuous supply of oocytes. However, our understanding of the molecular mechanisms that control the quiescence and activation of primordial follicles is still in its infancy. In this study, we provide some genetic evidence to show that the tumor suppressor tuberous sclerosis complex 2 (Tsc2), which negatively regulates mammalian target of rapamycin complex 1 (mTORC1), functions in oocytes to maintain the dormancy of primordial follicles. In mutant mice lacking the Tsc2 gene in oocytes, the pool of primordial follicles is activated prematurely due to elevated mTORC1 activity in oocytes. This results in depletion of follicles in early adulthood, causing premature ovarian failure (POF). Our results suggest that the Tsc1-Tsc2 complex mediated suppression of mTORC1 activity is indispensable for maintenance of the dormancy of primordial follicles, thus preserving the follicular pool, and that mTORC1 activity in oocytes promotes follicular activation. Our results also indicate that deregulation of Tsc/mTOR signaling in oocytes may cause pathological conditions of the ovary such as infertility and POF. © The Author 2009. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org.-
dc.languageeng-
dc.relation.ispartofMolecular Human Reproduction-
dc.subjectPremature ovarian failure-
dc.subjectOocytes-
dc.subjectFollicular activation-
dc.subjectTsc/mTOR signaling-
dc.titleDisruption of Tsc2 in oocytes leads to overactivation of the entire pool of primordial follicles-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/molehr/gap092-
dc.identifier.pmid19843635-
dc.identifier.scopuseid_2-s2.0-74049132482-
dc.identifier.volume15-
dc.identifier.issue12-
dc.identifier.spage765-
dc.identifier.epage770-
dc.identifier.eissn1460-2407-
dc.identifier.isiWOS:000271819000002-
dc.identifier.issnl1360-9947-

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