The developmental origins of the mammalian ovarian reserve

Grive, Kathryn J.; Freiman, Richard N.

doi:10.1242/dev.125211

Cited by 137 publications

(101 citation statements)

References 118 publications

(154 reference statements)

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“…The number of female germ cells, which comprises the “ovarian reserve”, reaches its peak during gestation and continues to decline during the reproductive lifespan of female mammals [105, 106]. It is now established that the ovarian reserve is established during gestation through a complex interplay between homeobox transcriptional factors, hormones, and genetic determinants, a process that can be disrupted by environmental factors through multiple mechanisms (reviewed by [105]). Some toxicants exert their action through induction of apoptosis during the breakdown of the germ cell nest, a critical step for establishing primordial follicles.…”

Section: Developmental Origins Of Adult Reproductive Dysfunction Amentioning

confidence: 99%

Environmental factors, epigenetics, and developmental origin of reproductive disorders

Cheong

Adgent

et al. 2017

Reproductive Toxicology

185

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Sex-specific differentiation, development, and function of the reproductive system are largely dependent on steroid hormones. For this reason, developmental exposure to estrogenic and anti-androgenic endocrine disrupting chemicals (EDCs) is associated with reproductive dysfunction in adulthood. Human data in support of “Developmental Origins of Health and Disease” (DOHaD) comes from multigenerational studies on offspring of diethylstilbestrol-exposed mothers/grandmothers. Animal data indicate that ovarian reserve, female cycling, adult uterine abnormalities, sperm quality, prostate disease, and mating behavior are susceptible to DOHaD effects induced by EDCs such as bisphenol A, genistein, diethylstilbestrol, p,p′-dichlorodiphenyl-dichloroethylene, phthalates, and polyaromatic hydrocarbons. Mechanisms underlying these EDC effects include direct mimicry of sex steroids or morphogens and interference with epigenomic sculpting during cell and tissue differentiation. Exposure to EDCs is associated with abnormal DNA methylation and other epigenetic modifications, as well as altered expression of genes important for development and function of reproductive tissues. Here we review the literature exploring the connections between developmental exposure to EDCs and adult reproductive dysfunction, and the mechanisms underlying these effects.

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Section: Developmental Origins Of Adult Reproductive Dysfunction Amentioning

confidence: 99%

Environmental factors, epigenetics, and developmental origin of reproductive disorders

Cheong

Adgent

et al. 2017

Reproductive Toxicology

185

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“…Meiosis in female mammals begins in the developing ovaries during the embryonic/fetal period arresting at the end of prophase I around or just after birth (De Felici, 2016). In mice, female PGCs colonize the gonadal ridges from E10.5 to E12.5 and after some rounds of mitotic division begin to enter meiosis between E13.5 and E14.5 (Grive & Freiman, 2015, Wang et al, 2017). During the mitosis-meiosis transition, germ cells undergo extensive changes in gene expression as they progress through the leptotene, zygotene, pachytene and diplotene stages until arresting at the dictyate stage of meiosis prophase I (Wang et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Dissecting the initiation of female meiosis in the mouse at single-cell resolution

Wang

Zhang

et al. 2019

Preprint

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ABSTRACTGerm cell meiosis is one of the most finely orchestrated events during gametogenesis with distinct developmental patterns in males and females. However, in mammals, the molecular mechanisms involved in this process remain not well known. Here, we report detailed transcriptome analyses of cell populations present in the mouse female gonadal ridges (E11.5) and the embryonic ovaries from E12.5 to E14.5 using single cell RNA sequencing (scRNA seq). These periods correspond with the initiation and progression of meiosis throughout the first stage of prophase I. We identified 13 transcriptionally distinct cell populations and 7 transcriptionally distinct germ cell subclusters that correspond to mitotic (3 clusters) and meiotic (4 clusters) germ cells. By comparing the signature gene expression pattern of 4 meiotic germ cell clusters, we found that the 4 cell clusters correspond to different cell status en route to meiosis progression, and therefore, our research here characterized detailed transcriptome dynamics during meiotic prophase I. Reconstructing the progression of meiosis along pseudotime, we identified several new genes and molecular pathways with potential critical roles in the mitosis/meiosis transition and early meiotic progression. Last, the heterogeneity within somatic cell populations was also discussed and different cellular states were identified. Our scRNA seq analysis here represents a new important resource for deciphering the molecular pathways driving meiosis initiation and progression in female germ cells and ovarian somatic cells.

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“…Meiotic cells were arrested in the diplotene stage of prophase I during germ cell cyst breakdown accompanied by reduction in cell numbers. Cyst breakdown is associated with the individualization of germ cells to form primordial oocytes, around 16 weeks of pregnancy in humans and at the time of birth in mice (Grive & Freiman 2015). Then, oocyte meiosis arrests in the dictyate stage of prophase I.…”

Section: Introductionmentioning

confidence: 99%

Disorganization of the germ cell pool leads to primary ovarian insufficiency

Kawashima

Kawamura

2017

Reproduction

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The mammalian ovary is an organ that controls female germ cell development, storing them and releasing mature oocytes for transporting to the oviduct. During the fetal stage, female germ cells change from a proliferative state to meiosis before forming follicles with the potential for the growth of surrounding somatic cells. Understanding of molecular and physiological bases of germ cell development in the fetal ovary contributed not only to the elucidation of genetic disorders in primary ovarian insufficiency (POI), but also to the advancement of novel treatments for patients with POI. Accumulating evidence indicates that mutations in NOBOX, DAZL and FIGLA genes are associated with POI. In addition, cell biology studies revealed the important roles of these genes as essential translational factors for germ cell development. Recent insights into the role of the PI3K (phosphatidylinositol 3-kinase)-AKT signaling pathway in primordial follicle activation allowed the development of a new infertility treatment, IVA (in vitro activation), leading to successful pregnancy/delivery in POI patients. Furthermore, elucidation of genetic dynamics underlying female germ cell development could allow regeneration of oocytes from ES (embryonic stem)/iPS (induced pluripotent stem) cells in mammals. The purpose of this review is to summarize basic findings related to female germ cell development and potential clinical implications, especially focusing on POI etiologies. We also summarize evolving new POI therapies based on IVA as well as oocyte regeneration.Reproduction (2017) 153 R205-R213

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The developmental origins of the mammalian ovarian reserve

Cited by 137 publications

References 118 publications

Environmental factors, epigenetics, and developmental origin of reproductive disorders

Environmental factors, epigenetics, and developmental origin of reproductive disorders

Dissecting the initiation of female meiosis in the mouse at single-cell resolution

Disorganization of the germ cell pool leads to primary ovarian insufficiency

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