ArticleChromosoma2019
ATR function is indispensable to allow proper mammalian follicle development.
Article in Chromosoma, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Acrylamide disrupts meiotic G2/M transition and SAC activity during oocyte maturation.Biology direct · 2026Article
- Article
- Regulation of Meiotic Prophase One in Mammalian Oocytes.Frontiers in cell and developmental biology · 2021Review
- Targeted Next-Generation Sequencing Indicates a Frequent Oligogenic Involvement in Primary Ovarian Insufficiency Onset.Frontiers in endocrinology · 2021Article
- The DNA damage response is required for oocyte cyst breakdown and follicle formation in mice.PLoS genetics · 2020Article
- Special issue on "recent advances in meiosis from DNA replication to chromosome segregation".Chromosoma · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian female fertility relies on the proper development of follicles. Right after birth in the mouse, oocytes associate with somatic ovarian cells to form follicles. These follicles grow during the adult lifetime to produce viable gametes. In this study, we analyzed the role of the ATM and rad3-related (ATR) kinase in mouse oogenesis and folliculogenesis using a hypomorphic mutation of the Atr gene (Murga et al. 2009). Female mice homozygotes for this allele have been reported to be sterile. Our data show that female meiotic prophase is not grossly altered when ATR levels are reduced. However, follicle development is substantially compromised, since Atr mutant ovaries present a decrease of growing follicles. Comprehensive analysis of follicular cell death and proliferation suggest that wild-type levels of ATR are required to achieve optimal follicular development. Altogether, these findings suggest that reduced ATR expression causes sterility due to defects in follicular progression rather than in meiotic recombination. We discuss the implications of these findings for the use of ATR inhibitors such as anti-cancer drugs and its possible side-effects on female fertility.
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Registered trials
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