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Journal articles on the topic 'Fetal germ cell'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Frazier, A. Lindsay, Christopher Weldon, and James Amatruda. "Fetal and neonatal germ cell tumors." Seminars in Fetal and Neonatal Medicine 17, no. 4 (2012): 222–30. http://dx.doi.org/10.1016/j.siny.2012.05.004.

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2

Western, P., J. Van Den Bergen, D. Miles, R. Ralli, and A. Sinclair. "002. REGULATION OF PLURIPOTENCY AND CELL CYCLE IN FETAL GERM CELLS." Reproduction, Fertility and Development 21, no. 9 (2009): 2. http://dx.doi.org/10.1071/srb09abs002.

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The germ cell lineage is unique in that it must ensure that the genome retains the complete developmental potential (totipotency) that supports development in the following generation. This is achieved through a number of mechanisms that prevent the early germ cell lineage from somatic differentiation and promote the capactity for functional totipotency. Part of this process involves the retained germ line expression of key genes that regulate pluripotency in embryonic stem cells, embryonic germ cells and some embryonal carcinoma cells, the stem cells of testicular tumours. Despite this, germ

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3

Angenard, Gaëlle, Vincent Muczynski, Hervé Coffigny, et al. "Cadmium Increases Human Fetal Germ Cell Apoptosis." Environmental Health Perspectives 118, no. 3 (2010): 331–37. http://dx.doi.org/10.1289/ehp.0900975.

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4

Isaacs, Hart. "Perinatal (fetal and neonatal) germ cell tumors." Journal of Pediatric Surgery 39, no. 7 (2004): 1003–13. http://dx.doi.org/10.1016/j.jpedsurg.2004.03.045.

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5

Lawaetz, Andreas C., and Kristian Almstrup. "Involvement of epigenetic modifiers in the pathogenesis of testicular dysgenesis and germ cell cancer." Biomolecular Concepts 6, no. 3 (2015): 219–27. http://dx.doi.org/10.1515/bmc-2015-0006.

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AbstractTesticular germ cell cancer manifests mainly in young adults as a seminoma or non-seminoma. The solid tumors are preceded by the presence of a non-invasive precursor cell, the carcinoma in situ cell (CIS), which shows great similarity to fetal germ cells. It is therefore hypothesized that the CIS cell is a fetal germ cell that has been arrested during development due to testicular dysgenesis. CIS cells retain a fetal and open chromatin structure, and recently several epigenetic modifiers have been suggested to be involved in testicular dysgenesis in mice. We here review the possible in

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6

van Vorstenbosch, C. J., E. Spek, B. Colenbrander, and C. J. Wensing. "The ultrastructure of normal fetal and neonatal pig testis germ cells and the influence of fetal decapitation on the germ cell development." Development 99, no. 4 (1987): 553–63. http://dx.doi.org/10.1242/dev.99.4.553.

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The development of germ cells in the male pig was investigated ultrastructurally in normal and decapitated fetuses. The age ranged respectively from 30 days p.c. till one month after birth and from 52 days p.c. until birth. The ultrastructural organization of the germ cells changes dramatically between 30 days p.c. and 52 days p.c. which coincides with the formation of ‘true’ sex cords. From 52 days p.c. onwards the morphology is rather stable: cells show a ‘hydrated’ appearance and typical cell bridges. There is no obvious difference in the ultrastructure of germ cells in decapitated animals,

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7

Childs, Andrew J., Philippa Saunders, and Richard A. Anderson. "Modeling Human Fetal Germ Cell Development In Vitro." Biology of Reproduction 78, Suppl_1 (2008): 300. http://dx.doi.org/10.1093/biolreprod/78.s1.300.

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8

Chappell, Vesna A., Brett D. Keiper, and Christopher B. Geyer. "Translational Control During Fetal Male Germ Cell Development." Biology of Reproduction 87, Suppl_1 (2012): 137. http://dx.doi.org/10.1093/biolreprod/87.s1.137.

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9

De Felici, Massimo, Francesca Klinger, Federica Campolo, Carmela Balistreri, Marco Barchi, and Susanna Dolci. "To Be or Not to Be a Germ Cell: The Extragonadal Germ Cell Tumor Paradigm." International Journal of Molecular Sciences 22, no. 11 (2021): 5982. http://dx.doi.org/10.3390/ijms22115982.

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In the human embryo, the genetic program that orchestrates germ cell specification involves the activation of epigenetic and transcriptional mechanisms that make the germline a unique cell population continuously poised between germness and pluripotency. Germ cell tumors, neoplasias originating from fetal or neonatal germ cells, maintain such dichotomy and can adopt either pluripotent features (embryonal carcinomas) or germness features (seminomas) with a wide range of phenotypes in between these histotypes. Here, we review the basic concepts of cell specification, migration and gonadal coloni

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10

Spiller, Cassy M., Josephine Bowles, and Peter Koopman. "Nodal/Cripto signaling in fetal male germ cell development: implications for testicular germ cell tumors." International Journal of Developmental Biology 57, no. 2-3-4 (2013): 211–19. http://dx.doi.org/10.1387/ijdb.130028pk.

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11

De Felici, Massimo, Susanna Dolci, and Gregorio Siracusa. "Fetal germ cells establish cell coupling with follicle cells in vitro." Cell Differentiation and Development 28, no. 1 (1989): 65–69. http://dx.doi.org/10.1016/0922-3371(89)90024-5.

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12

Jørgensen, Anne, and Ewa Rajpert-De Meyts. "Regulation of meiotic entry and gonadal sex differentiation in the human: normal and disrupted signaling." Biomolecular Concepts 5, no. 4 (2014): 331–41. http://dx.doi.org/10.1515/bmc-2014-0014.

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AbstractMeiosis is a unique type of cell division that is performed only by germ cells to form haploid gametes. The switch from mitosis to meiosis exhibits a distinct sex-specific difference in timing, with female germ cells entering meiosis during fetal development and male germ cells at puberty when spermatogenesis is initiated. During early fetal development, bipotential primordial germ cells migrate to the forming gonad where they remain sexually indifferent until the sex-specific differentiation of germ cells is initiated by cues from the somatic cells. This irreversible step in gonadal s

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13

Mishra, Swati, Jasin Taelman, Yolanda W. Chang, et al. "Sex-Specific Isolation and Propagation of Human Premeiotic Fetal Germ Cells and Germ Cell-Like Cells." Cells 10, no. 5 (2021): 1214. http://dx.doi.org/10.3390/cells10051214.

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The second trimester of human development is marked by asynchronous gonadal development hampering the isolation of homogenous populations of early and late fetal germ cells (FGCs). We evaluated the feasibility of using surface markers TNAP, PDPN, EPCAM and ITGA6 to isolate FGCs as well as human primordial germ cell-like cells (hPGCLCs) derived from embryonic stem cells (hESCs) from both sexes by fluorescence-activated cell sorting (FACS). Our results suggest that a combination of TNAP and PDPN was sufficient to separate populations of premeiotic FGCs and hPGCLCs in both sexes. This combination

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14

Nettersheim, Daniel, Sina Jostes, Simon Schneider, and Hubert Schorle. "Elucidating human male germ cell development by studying germ cell cancer." Reproduction 152, no. 4 (2016): R101—R113. http://dx.doi.org/10.1530/rep-16-0114.

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Human germ cell development is regulated in a spatio-temporal manner by complex regulatory networks. Here, we summarize results obtained in germ cell tumors and respective cell lines and try to pinpoint similarities to normal germ cell development. This comparison allows speculating about the critical and error-prone mechanisms, which when disturbed, lead to the development of germ cell tumors. Short after specification, primordial germ cells express markers of pluripotency, which, in humans, persists up to the stage of fetal/infantile spermatogonia. Aside from the rare spermatocytic tumors, v

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15

Souquet, Benoit, Sophie Tourpin, Sébastien Messiaen, Delphine Moison, René Habert, and Gabriel Livera. "Nodal Signaling Regulates the Entry into Meiosis in Fetal Germ Cells." Endocrinology 153, no. 5 (2012): 2466–73. http://dx.doi.org/10.1210/en.2011-2056.

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The mechanisms regulating the entry into meiosis in mammalian germ cells remain incompletely understood. We investigated the involvement of the TGF-β family members in fetal germ cell meiosis initiation. Nodal, a member of the TGF-β family, and its target genes are precociously expressed in embryonic gonads and show sexual dimorphism in favor of the developing testis. Nodal receptor genes, Acvr2a and Acvr2b, Alk4, and Tdgf1/Cripto, were identified in male germ cells. Nodal itself, Tdgf1, and Lefty1 and Lefty2 are targets of Nodal signaling and were all found specifically expressed in male germ

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16

Scarlet, Dragos, Stephan Handschuh, Ursula Reichart, et al. "Sexual Differentiation and Primordial Germ Cell Distribution in the Early Horse Fetus." Animals 11, no. 8 (2021): 2422. http://dx.doi.org/10.3390/ani11082422.

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It was the aim of this study to characterize the development of the gonads and genital ducts in the equine fetus around the time of sexual differentiation. This included the identification and localization of the primordial germ cell population. Equine fetuses between 45 and 60 days of gestation were evaluated using a combination of micro-computed tomography scanning, immunohistochemistry, and multiplex immunofluorescence. Fetal gonads increased in size 23-fold from 45 to 60 days of gestation, and an even greater increase was observed in the metanephros volume. Signs of mesonephros atrophy wer

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17

Hayashi, Yohei, Masaru Mori, Kaori Igarashi, et al. "Proteomic and metabolomic analyses uncover sex-specific regulatory pathways in mouse fetal germline differentiation†." Biology of Reproduction 103, no. 4 (2020): 717–35. http://dx.doi.org/10.1093/biolre/ioaa115.

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Abstract Regulatory mechanisms of germline differentiation have generally been explained via the function of signaling pathways, transcription factors, and epigenetic regulation; however, little is known regarding proteomic and metabolomic regulation and their contribution to germ cell development. Here, we conducted integrated proteomic and metabolomic analyses of fetal germ cells in mice on embryonic day (E)13.5 and E18.5 and demonstrate sex- and developmental stage-dependent changes in these processes. In male germ cells, RNA processing, translation, oxidative phosphorylation, and nucleotid

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18

Benbrahim-Tallaa, Lamia, Bénazir Siddeek, Aline Bozec, et al. "Alterations of Sertoli cell activity in the long-term testicular germ cell death process induced by fetal androgen disruption." Journal of Endocrinology 196, no. 1 (2007): 21–31. http://dx.doi.org/10.1677/joe-07-0062.

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Fetal androgen disruption, induced by the administration of anti-androgen flutamide (0.4, 2, and 10 mg/kg day) causes a long-term apoptosis in testicular germ cells in adult male rat offspring. One of the questions raised by this observation is the role of the Sertoli cells in the adult germ cell apoptotic process. It is shown here that Sertoli cells originating from 15-day-old rats treated in utero with the anti-androgen (10 mg/kg d) did no longer protect adult germ cells against apoptosis. Indeed, untreated spermatocytes or spermatids exhibited increased (P<0.0001) active caspase-3 levels

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19

Spiller, Cassy M., Josephine Bowles, and Peter Koopman. "Regulation of germ cell meiosis in the fetal ovary." International Journal of Developmental Biology 56, no. 10-11-12 (2012): 779–87. http://dx.doi.org/10.1387/ijdb.120142pk.

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20

Moens, André, Bernadette Fléchon, Jéril Degrouard, et al. "Ultrastructural and immunocytochemical analysis of diploid germ cells isolated from fetal rabbit gonads." Zygote 5, no. 1 (1997): 47–60. http://dx.doi.org/10.1017/s0967199400003555.

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SummaryGerm cells were isolated from rabbit fetal gonads between 18 and 22 days post coitum and examined morphologically, ultrastructurally and for immunocytochemical and cytochemical characteristics. Observations were compared with the information available from the corresponding cells of other mammalian species. The general morphology and ultrastructure of healthy isolated rabbit fetal germ cells were found to be very similar to those of the rabbit and mouse diploid germ cells in situ. Moreover, rabbit fetal germ cells shared common immunocytochemical characteristics with mouse undifferentia

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21

Poulain, Marine, Nelly Frydman, Clotilde Duquenne, et al. "Dexamethasone Induces Germ Cell Apoptosis in the Human Fetal Ovary." Journal of Clinical Endocrinology & Metabolism 97, no. 10 (2012): E1890—E1897. http://dx.doi.org/10.1210/jc.2012-1681.

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Abstract Context: The 21-hydroxylase deficiency is the most common cause of congenital adrenal hyperplasia. Pregnant women presenting a risk of genetic transmission may be treated with synthetic glucocorticoids such as dexamethasone (DEX) to prevent female fetus virilization. Objective: The aim of this study was to assess the potential deleterious effects of DEX exposure on fetal ovarian development. Settings: Human fetal ovaries, ranging from 8–11 weeks after fertilization, were harvested from material available after legally induced abortions. They were cultured in the absence or presence of

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22

Scarlet, D., U. Reichart, G. Podico, et al. "57 Primordial germ cell distribution in the horse fetal gonad." Reproduction, Fertility and Development 32, no. 2 (2020): 154. http://dx.doi.org/10.1071/rdv32n2ab57.

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Germ cell development and differentiation is a complex process associated with down-regulation of stem cell-associated genes and up-regulation of markers of germ cell differentiation and meiosis. In horses, putative primordial germ cells (PGCs) were identified outside the gonads starting 20 days after ovulation (Curran et al. 1997 Equine Vet. J. Suppl. 25, 72-76). However, no information is available after the time when these cells enter the gonad. The aim of this study was to identify, localise, and quantify PGCs in fetal male and female gonads. Twelve (5 males and 7 females) equine fetuses w

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23

Nwachukwu, Chinwe U., Kathryn J. Woad, Nicole Barnes, David S. Gardner, and Robert S. Robinson. "Maternal protein restriction affects fetal ovary development in sheep." Reproduction and Fertility 2, no. 2 (2021): 161–71. http://dx.doi.org/10.1530/raf-20-0073.

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Maternal malnutrition has important developmental consequences for the foetus. Indeed, adverse fetal ovarian development could have lifelong impact, with potentially reduced ovarian reserve and fertility of the offspring. This study investigated the effect of maternal protein restriction on germ cell and blood vessel development in the fetal sheep ovary. Ewes were fed control (n = 7) or low protein (n = 8) diets (17.0 g vs 8.7 g crude protein/MJ metabolizable energy) from conception to day 65 of gestation (gd65). On gd65, fetal ovaries were subjected to histological and immunohistochemical ana

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Yoo, J. M., J. J. Park, K. Gobianand, et al. "217 PROTEIN-INDUCED TRANSDIFFERENTIATION INTO MALE GERM CELL-LIKE LINEAGE FROM CHICKEN FETAL BONE MARROW STEM CELLS." Reproduction, Fertility and Development 24, no. 1 (2012): 220. http://dx.doi.org/10.1071/rdv24n1ab217.

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Bone marrow (BM)-derived stem cells are capable of transdifferentiation into multilineage cells like muscle, bone, cartilage, fat and nerve cells. In this study, we investigated the capability of mesenchymal stem cells (MSC) derived from BM into germ cell differentiation in the chicken. Chicken MSCs were isolated from BM of day 20 fertilized fetal chicken with Ficoll-Paque Plus. Isolated cells were cultured in advance-DMEM (ADMEM) supplemented with 10% fetal bovine serum and antibiotics. Once confluent, cells were subcultured until five passages. The cultured cells showed fibroblast-like morph

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25

Wu, Ji, Yi Chen, and Tan Li. "Expression of Fas, p53 and AFP in development of human fetal germ cells in vitro." Zygote 10, no. 4 (2002): 333–40. http://dx.doi.org/10.1017/s0967199402004070.

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In the present study we employed a two-step culture system to study the expression of Fas, p53 and alpha-fetoprotein (AFP) in the development in vitro of human fetal germ cells. p53 mRNA was determined by Northern blotting, and Fas content was assessed by western blotting. RT-nested polymerase chain reaction (RT-nPCR) analysis was performed to determine the expression of AFP mRNA in different stages of fetal follicular development. Follicular cell apoptosis was evaluated by DNA fragmentation analyses (DNA ladder). The results showed that by day 7 of culture approximately one-sixth of fetal ger

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26

Kawashima, Ikko, and Kazuhiro Kawamura. "Disorganization of the germ cell pool leads to primary ovarian insufficiency." Reproduction 153, no. 6 (2017): R205—R213. http://dx.doi.org/10.1530/rep-17-0015.

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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. Accumu

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27

Shah, Syed Mohmad, Neha Saini, Syma Ashraf, et al. "Cumulus cell-conditioned medium supports embryonic stem cell differentiation to germ cell-like cells." Reproduction, Fertility and Development 29, no. 4 (2017): 679. http://dx.doi.org/10.1071/rd15159.

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Cumulus cells provide cellular interactions and growth factors required for oogenesis. In vitro studies of oogenesis are limited primarily because of the paucity of their source, first trimester fetal gonads, and the small number of germ lineage precursor cells present within these tissues. In order to understand this obscure but vitally important process, the present study was designed to direct differentiation of embryonic stem (ES) cells into germ lineage cells. For this purpose, buffalo ES cells were differentiated, as embryoid bodies (EBs) and monolayer adherent cultures, in the presence

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28

Urven, Lance E., David E. Weng, Annabel L. Schumaker, John D. Gearhart, and John R. Mccarrey. "Differential Gene Expression in Fetal Mouse Germ Cells1." Biology of Reproduction 48, no. 3 (1993): 564–74. http://dx.doi.org/10.1095/biolreprod48.3.564.

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29

Spiller, Cassy, Dagmar Wilhelm, and Peter Koopman. "Cell cycle analysis of fetal germ cells during sex differentiation in mice." Biology of the Cell 101, no. 10 (2009): 587–98. http://dx.doi.org/10.1042/bc20090021.

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30

Kato, Y., and Y. Tsunoda. "Nuclear transplantation of mouse fetal germ cells into enucleated two-cell embryos." Theriogenology 37, no. 4 (1992): 769–78. http://dx.doi.org/10.1016/0093-691x(92)90040-x.

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31

Dolci, S., and M. De Felici. "A study of meiosis in chimeric mouse fetal gonads." Development 109, no. 1 (1990): 37–40. http://dx.doi.org/10.1242/dev.109.1.37.

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The influence of somatic environment on the onset and progression of meiosis in fetal germ cells was studied in chimeric gonads produced in vitro by dissociation-reaggregation experiments. Germ cells isolated from testes or ovaries of 11.5-13.5 days post coitum (dpc) CD-1 mouse embryos were loaded with the fluorescent supravital dye 5–6 carboxyfluorescein diacetate succinimyl ester (CFSE) and mixed with a cell suspension obtained by trypsin-EDTA treatment of gonads of various ages and of the same or opposite sex. Whereas 11.5 dpc donor germ cells appeared unable to survive in the chimeric gona

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32

Konkel, Lindsey. "Uncomfortable Uncertainty: Do OTC Analgesics Disrupt Fetal Germ Cell Development?" Environmental Health Perspectives 126, no. 9 (2018): 094001. http://dx.doi.org/10.1289/ehp3799.

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33

Rolland, A. D., K. P. Lehmann, K. J. Johnson, K. W. Gaido, and P. Koopman. "Uncovering Gene Regulatory Networks During Mouse Fetal Germ Cell Development." Biology of Reproduction 84, no. 4 (2010): 790–800. http://dx.doi.org/10.1095/biolreprod.110.088443.

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34

Gashaw, I., O. Dushaj, R. Behr, et al. "Novel germ cell markers characterize testicular seminoma and fetal testis." Molecular Human Reproduction 13, no. 10 (2007): 721–27. http://dx.doi.org/10.1093/molehr/gam059.

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35

Honecker, Friedemann, Anne-Marie F. Kersemaekers, Michel Molier та ін. "Involvement of E-cadherin andβ-catenin in germ cell tumours and in normal male fetal germ cell development". Journal of Pathology 204, № 2 (2004): 167–74. http://dx.doi.org/10.1002/path.1614.

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36

Bahena, I., E. Xu, M. Betancourt, et al. "Role of Mael in early oogenesis and during germ-cell differentiation from embryonic stem cells in mice in vitro." Zygote 22, no. 4 (2013): 513–20. http://dx.doi.org/10.1017/s0967199412000743.

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SummaryIn a previous study, we have identified a set of conserved spermatogenic genes whose expression is restricted to testis and ovary and that are developmentally regulated. One of these genes, the transcription factor Mael, has been reported to play an essential role in mouse spermatogenesis. Nevertheless, the role of Mael in mouse oogenesis has not been defined. In order to analyse the role of Mael in mouse oogenesis, the expression of this gene was blocked during early oogenesis in mouse in vitro using RNAi technology. In addition, the role of Mael during differentiation of embryonic ste

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37

Shen, Wei, Lan Li, Zhaodai Bai, Qingjie Pan, Mingxiao Ding, and Hongkui Deng. "In vitro development of mouse fetal germ cells into mature oocytes." Reproduction 134, no. 2 (2007): 223–31. http://dx.doi.org/10.1530/rep-06-0378.

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Little is known about the mechanisms underlying primordial follicular formation and the acquisition of competence to resume meiosis by growing oocytes. It is therefore important to establish anin vitroexperimental model that allows one to study such mechanisms. Mouse follicular development has been studiedin vitroover the past several years; however, no evidence has been presented showing that mature oocytes can be obtained from mouse fetal germ cells prior to the formation of primordial follicles. In this study, a method has been established to obtain mature oocytes from the mouse fetal germ

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38

Looijenga, Leendert, Hendrik Wermann, Hans Stoop, et al. "Gobal DNA methylation in fetal human germ cells and germ cell tumors: correlation with differentiation and cisplatin resistance." Cancer Genetics and Cytogenetics 203, no. 1 (2010): 64. http://dx.doi.org/10.1016/j.cancergencyto.2010.07.045.

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39

Salonen, Jonna, Ewa Rajpert-De Meyts, Susanna Mannisto, et al. "Differential developmental expression of transcription factors GATA-4 and GATA-6, their cofactor FOG-2 and downstream target genes in testicular carcinoma in situ and germ cell tumors." European Journal of Endocrinology 162, no. 3 (2010): 625–31. http://dx.doi.org/10.1530/eje-09-0734.

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ObjectiveTesticular germ cell cancer is the most common malignancy among young males. The pre-invasive precursor, carcinoma in situ testis (CIS), presumably originates from arrested and transformed fetal gonocytes. Given that GATA transcription factors have essential roles in embryonic and testicular development, we explored the expression of GATA-4, GATA-6, cofactor friend of GATA (FOG)-2, and downstream target genes during human testis development and addressed the question whether changes in this pathway may contribute to germ cell neoplasms.MethodsFetal testis, testicular CIS, and overt tu

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Yamazaki, Yukiko, Hideki Sakamoto, Samuel Kor, Yuuki Maeda, and Nathanael C. Hogg. "Sex-Specific Gene Knockdown in Mouse Fetal Germ Cells." Biology of Reproduction 87, Suppl_1 (2012): 203. http://dx.doi.org/10.1093/biolreprod/87.s1.203.

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41

Monk, M., M. Boubelik, and S. Lehnert. "Temporal and regional changes in DNA methylation in the embryonic, extraembryonic and germ cell lineages during mouse embryo development." Development 99, no. 3 (1987): 371–82. http://dx.doi.org/10.1242/dev.99.3.371.

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This paper shows stage- and tissue-specific global demethylation and remethylation occurring during embryonic development. The egg genome is strikingly undermethylated and the sperm genome relatively methylated. Following a loss of genomic methylation during preimplantation development, embryonic and extraembryonic lineages are progressively and independently methylated to different final extents. Methylation continues postgastrulation and hence could be a mechanism initiating, or confirming, differential programming in the definitive germ layers. It is proposed that much of the methylation ob

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42

Wang, Rui-An, Paul K. Nakane, and Takehiko Koji. "Autonomous Cell Death of Mouse Male Germ Cells during Fetal and Postnatal Period1." Biology of Reproduction 58, no. 5 (1998): 1250–56. http://dx.doi.org/10.1095/biolreprod58.5.1250.

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43

Panula, Sarita, Jose V. Medrano, Kehkooi Kee, et al. "Human germ cell differentiation from fetal- and adult-derived induced pluripotent stem cells." Human Molecular Genetics 20, no. 4 (2010): 752–62. http://dx.doi.org/10.1093/hmg/ddq520.

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44

Nguyen, Daniel H., Bikem Soygur, Su-Ping Peng, Safia Malki, Guang Hu, and Diana J. Laird. "Apoptosis in the fetal testis eliminates developmentally defective germ cell clones." Nature Cell Biology 22, no. 12 (2020): 1423–35. http://dx.doi.org/10.1038/s41556-020-00603-8.

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45

Trautmann, Emilie, Marie-Justine Guerquin, Clotilde Duquenne, Jean-Baptiste Lahaye, René Habert, and Gabriel Livera. "Retinoic acid prevents germ cell mitotic arrest in mouse fetal testes." Cell Cycle 7, no. 5 (2008): 656–64. http://dx.doi.org/10.4161/cc.7.5.5482.

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46

Ross, A., S. Munger, and B. Capel. "Bmp7 Regulates Germ Cell Proliferation in Mouse Fetal Gonads." Sexual Development 1, no. 2 (2007): 127–37. http://dx.doi.org/10.1159/000100034.

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47

Kurishima, Clara, Masaki Wada, Masato Sakai, et al. "Congenital brain tumor: Fetal case of congenital germ cell intracranial tumor." Pediatrics International 54, no. 2 (2012): 282–85. http://dx.doi.org/10.1111/j.1442-200x.2011.03465.x.

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48

Modi, D. N. "Accelerated germ cell apoptosis in sex chromosome aneuploid fetal human gonads." Molecular Human Reproduction 9, no. 4 (2003): 219–25. http://dx.doi.org/10.1093/molehr/gag031.

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49

Coutts, S. M., N. Fulton, and R. A. Anderson. "Environmental toxicant-induced germ cell apoptosis in the human fetal testis." Human Reproduction 22, no. 11 (2007): 2912–18. http://dx.doi.org/10.1093/humrep/dem300.

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Rodrigues, Patricia, Darlene Limback, Lynda K. McGinnis, Carlos E. Plancha, and David F. Albertini. "Multiple mechanisms of germ cell loss in the perinatal mouse ovary." REPRODUCTION 137, no. 4 (2009): 709–20. http://dx.doi.org/10.1530/rep-08-0203.

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Abstract:

In the perinatal ovary of most mammals, external and internal factors establish a primordial follicle reserve that specifies the duration of the reproductive lifespan of a given species. We analyzed the mechanism of follicle loss and survival in C57BI/6 mice using static and dynamic assays of apoptosis, autophagy, and ovarian morphogenesis. We confirm an initial loss soon after birth, when about 44% of the germ cells detectable at the end of the fetal period abruptly disappear. The observations that (1) few germ or somatic cells were apoptotic in newborn ovaries, (2) vitally stained organ cult

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