ArticlePLoS genetics2015
Inactivation of Retinoblastoma Protein (Rb1) in the Oocyte: Evidence That Dysregulated Follicle Growth Drives Ovarian Teratoma Formation in Mice.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- A rare germline BMP15 missense mutation causes hereditary ovarian immature teratoma in human.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- STRA8-RB interaction is required for timely entry of meiosis in mouse female germ cells.Nature communications · 2023Article
- Regulation of adult stem cell quiescence and its functions in the maintenance of tissue integrity.Nature reviews. Molecular cell biology · 2023Review
- Deconstructing a Syndrome: Genomic Insights Into PCOS Causal Mechanisms and Classification.Endocrine reviews · 2022Article
- Multiomic analysis identifies CPT1A as a potential therapeutic target in platinum-refractory, high-grade serous ovarian cancer.Cell reports. Medicine · 2021Article
- Proper timing of a quiescence period in precursor prospermatogonia is required for stem cell pool establishment in the male germline.Development (Cambridge, England) · 2021Article
- MC4R mutant mice develop ovarian teratomas.Scientific reports · 2021Article
- Distinct subtypes of polycystic ovary syndrome with novel genetic associations: An unsupervised, phenotypic clustering analysis.PLoS medicine · 2020Article
- Article
- Family-Based Quantitative Trait Meta-Analysis Implicates Rare Noncoding Variants in DENND1A in Polycystic Ovary Syndrome.The Journal of clinical endocrinology and metabolism · 2019Article
- Dnd1-mediated epigenetic control of teratoma formation in mouse.Biology open · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The origin of most ovarian tumors is undefined. Here, we report development of a novel mouse model in which conditional inactivation of the tumor suppressor gene Rb1 in oocytes leads to the formation of ovarian teratomas (OTs). While parthenogenetically activated ooctyes are a known source of OT in some mutant mouse models, enhanced parthenogenetic propensity in vitro was not observed for Rb1-deficient oocytes. Further analyses revealed that follicle recruitment and growth is disrupted in ovaries of mice with conditional inactivation of Rb1, leading to abnormal accumulation of secondary/preantral follicles. These findings underpin the concept that miscues between the germ cell and somatic compartments cause premature oocyte activation and the formation of OTs. Furthermore, these results suggest that defects in folliculogenesis and a permissive genetic background are sufficient to drive OT development, even in the absence of enhanced parthenogenetic activation. Thus, we have discovered a novel role of Rb1 in regulating the entry of primordial oocytes into the pool of growing follicles and signaling between the oocyte and granulosa cells during the protracted process of oocyte growth. Our findings, coupled with data from studies of other OT models, suggest that defects in the coordinated regulation between growth of the oocyte and somatic components in follicles are an underlying cause of OT formation.
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