WOMEN IN REPRODUCTIVE SCIENCE: To be or not to be a testis

Capel, Blanche

doi:10.1530/rep-19-0151

Cited by 10 publications

(5 citation statements)

References 104 publications

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“…Soon after sex determination in mammals, embryonic female and male germ cells receive distinct signals to initiate a sex-specific germ cell differentiation program ( Capel, 2019 ). However, it is unclear how these newly defined germ cells integrate external signals to execute precise and sex-specific gene expression programs and cell cycle states required for germ cell development.…”

Section: Discussionmentioning

confidence: 99%

Transcription and chromatin regulation by TAF4b during cellular quiescence of developing prospermatogonia

Gura,

Bartholomew,

Abt

et al. 2023

Front. Cell Dev. Biol.

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Prospermatogonia (ProSpg) link the embryonic development of male primordial germ cells to the healthy establishment of postnatal spermatogonia and spermatogonial stem cells. While these spermatogenic precursor cells undergo the characteristic transitions of cycling and quiescence, the transcriptional events underlying these developmental hallmarks remain unknown. Here, we investigated the expression and function of TBP-associated factor 4b (Taf4b) in the timely development of quiescent mouse ProSpg using an integration of gene expression profiling and chromatin mapping. We find that Taf4b mRNA expression is elevated during the transition of mitotic-to-quiescent ProSpg and Taf4b-deficient ProSpg are delayed in their entry into quiescence. Gene ontology, protein network analysis, and chromatin mapping demonstrate that TAF4b is a direct and indirect regulator of chromatin and cell cycle-related gene expression programs during ProSpg quiescence. Further validation of these cell cycle mRNA changes due to the loss of TAF4b was accomplished via immunostaining for proliferating cell nuclear antigen (PCNA). Together, these data indicate that TAF4b is a key transcriptional regulator of the chromatin and quiescent state of the developing mammalian spermatogenic precursor lineage.

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Section: Discussionmentioning

confidence: 99%

Transcription and chromatin regulation by TAF4b during cellular quiescence of developing prospermatogonia

Gura,

Bartholomew,

Abt

et al. 2023

Front. Cell Dev. Biol.

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“…It is generally considered that these processes are largely conserved between mice and humans although there appear to be some exceptions to this notion. With the use of knockout mouse models, the signalling pathways and mechanisms controlling sex-specific differentiation of the bipotential gonad has been extensively studied in recent years (reviewed in detail in Wilhelm et al, 2007 ; Greenfield, 2015 ; Lin and Capel, 2015 ; Rotgers et al, 2018 ; Yang et al, 2018 ; Capel, 2019 ; Nef et al, 2019 ; Yildirim et al, 2020 )). In brief, the presence of the Sex-determining Region Y (SRY) gene, expressed from the Y-chromosome at embryonic day (E) 10.5, initiates Sertoli cell differentiation from the supporting cell lineage ( Koopman et al, 1990 ; Bullejos and Koopman, 2001 ).…”

Section: Brief Overview Of Sex-specific Gonadal Differentiation In Micementioning

confidence: 99%

Deciphering Sex-Specific Differentiation of Human Fetal Gonads: Insight From Experimental Models

Riis

Jørgensen

2022

Front. Cell Dev. Biol.

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Sex-specific gonadal differentiation is initiated by the expression of SRY in male foetuses. This promotes a signalling pathway directing testicular development, while in female foetuses the absence of SRY and expression of pro-ovarian factors promote ovarian development. Importantly, in addition to the initiation of a sex-specific signalling cascade the opposite pathway is simultaneously inhibited. The somatic cell populations within the gonads dictates this differentiation as well as the development of secondary sex characteristics via secretion of endocrine factors and steroid hormones. Opposing pathways SOX9/FGF9 (testis) and WNT4/RSPO1 (ovary) controls the development and differentiation of the bipotential mouse gonad and even though sex-specific gonadal differentiation is largely considered to be conserved between mice and humans, recent studies have identified several differences. Hence, the signalling pathways promoting early mouse gonad differentiation cannot be directly transferred to human development thus highlighting the importance of also examining this signalling in human fetal gonads. This review focus on the current understanding of regulatory mechanisms governing human gonadal sex differentiation by combining knowledge of these processes from studies in mice, information from patients with differences of sex development and insight from manipulation of selected signalling pathways in ex vivo culture models of human fetal gonads.

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“…The Y chromosome contains only 50 to 60 unique protein-coding genes that encode primarily for molecules required for gonadal formation and fertility, including the Sry gene, which is necessary for the development of male gonads ( 145 ) and the Azf (azoospermia factor) locus that has a role in organs outside the testis, including the brain ( 146 ), and in inflammation ( 147 , 148 ). Variable amounts of gene replication occur on the Y chromosome from different species, so that the Y chromosomes from humans and mice are quite different ( 149 , 150 ).…”

Section: Role Of Sex Chromosomes and Sex Hormones In Sexual Dimorphis...mentioning

confidence: 99%

Effects of biological sex and pregnancy in experimental autoimmune encephalomyelitis: It’s complicated

McCombe

Greer

2022

Front. Immunol.

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Experimental autoimmune encephalomyelitis (EAE) can be induced in many animal strains by inoculation with central nervous system antigens and adjuvant or by the passive transfer of lymphocytes reactive with these antigens and is widely used as an animal model for multiple sclerosis (MS). There are reports that female sex and pregnancy affect EAE. Here we review the effects of biological sex and the effects of pregnancy on the clinical features (including disease susceptibility) and pathophysiology of EAE. We also review reports of the possible mechanisms underlying these differences. These include sex-related differences in the immune system and in the central nervous system, the effects of hormones and the sex chromosomes and molecules unique to pregnancy. We also review sex differences in the response to factors that can modify the course of EAE. Our conclusion is that the effects of biological sex in EAE vary amongst animal models and should not be widely extrapolated. In EAE, it is therefore essential that studies looking at the effects of biological sex or pregnancy give full information about the model that is used (i.e. animal strain, sex, the inducing antigen, timing of EAE induction in relation to pregnancy, etc.). In addition, it would be preferable if more than one EAE model were used, to show if any observed effects are generalizable. This is clearly a field that requires further work. However, understanding of the mechanisms of sex differences could lead to greater understanding of EAE, and suggest possible therapies for MS.

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WOMEN IN REPRODUCTIVE SCIENCE: To be or not to be a testis

Cited by 10 publications

References 104 publications

Transcription and chromatin regulation by TAF4b during cellular quiescence of developing prospermatogonia

Transcription and chromatin regulation by TAF4b during cellular quiescence of developing prospermatogonia

Deciphering Sex-Specific Differentiation of Human Fetal Gonads: Insight From Experimental Models

Effects of biological sex and pregnancy in experimental autoimmune encephalomyelitis: It’s complicated

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