scholarly journals Differential effects of testosterone and 17β-estradiol on gonadal development in five anuran species

Reproduction ◽  
2012 ◽  
Vol 144 (2) ◽  
pp. 257-267 ◽  
Author(s):  
Rafał P Piprek ◽  
Anna Pecio ◽  
Jacek Z Kubiak ◽  
Jacek M Szymura
Keyword(s):  
Sex Determination ◽  
Sex Steroids ◽  
Gonadal Development ◽  
Sex Reversal ◽  
Differential Sensitivity ◽  
Anuran Species ◽  
Hyla Arborea ◽  
Gonad Differentiation ◽  
Bombina Variegata ◽  
17Β Estradiol

Sex hormones are essential for sexual differentiation and play a key role in the development of gonads in amphibians. The goal of this study was to evaluate the influence of exogenous sex steroids, testosterone, and 17β-estradiol (E2) on development of gonads in five anuran species differing in their evolutionary positions, sex determination, and mode of gonadogenesis. We found that in two closely related species of fire-bellied toad, Bombina bombina and Bombina variegata, testosterone and E2 exposure results in sex reversal as well as intersex and undifferentiated gonads. Similarly, sex reversal was observed in Hyla arborea after exposure to male or female sex steroids. Xenopus laevis was sensitive to E2 but only moderately to testosterone. In Bufo viridis, treatment with either sex hormone provoked a developmental delay in gonads and Bidder's organs. Therefore, susceptibility to hormonal sex reversal appeared species dependent but unrelated to genetic sex determination and the type of gonadogenesis. We also found that the onset of sex steroid exposure influences gonad differentiation and the meiotic status of the germ cells depends on their location within the gonad. Our findings reveal differential sensitivity of amphibians to testosterone and E2, establishing a hierarchy of sensitivity to these hormones among different anuran species.

scholarly journals TET2 catalyzes active DNA demethylation of the Sry promoter and enhances its expression

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Naoki Okashita ◽  
Shunsuke Kuroki ◽  
Ryo Maeda ◽  
Makoto Tachibana
Keyword(s):  
Sex Determination ◽  
Gonadal Development ◽  
Sex Reversal ◽  
Dna Demethylation ◽  
Active Dna Demethylation ◽  
Specific Manner ◽  
Male Sex ◽  
Male To Female ◽  
Deficient Mice

Abstract SRY is the master regulator of male sex determination in eutherian mammals. In mice, Sry expression is transcriptionally and epigenetically controlled in a developmental stage-specific manner. The Sry promoter undergoes demethylation in embryonic gonadal somatic cells at the sex-determining period. However, its molecular mechanism and in vivo significance remain unclear. Here, we report that the Sry promoter is actively demethylated during gonadal development, and TET2 plays a fundamental role in Sry demethylation. Tet2-deficient mice showed absence of 5-hydroxymethylcytosine in the Sry promoter. Furthermore, Tet2 deficiency diminished Sry expression, indicating that TET2-mediated DNA demethylation regulates Sry expression positively. We previously showed that the deficiency of the H3K9 demethylase Jmjd1a compromises Sry expression and induces male-to-female sex reversal. Tet2 deficiency enhanced the sex reversal phenotype of Jmjd1a-deficient mice. Thus, TET2-mediated active DNA demethylation and JMJD1A-mediated H3K9 demethylation contribute synergistically to sex determination.

scholarly journals Diverse Regulation but Conserved Function: SOX9 in Vertebrate Sex Determination

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 486
Author(s):  
Brittany Vining ◽  
Zhenhua Ming ◽  
Stefan Bagheri-Fam ◽  
Vincent Harley
Keyword(s):  
Sex Determination ◽  
Molecular Switches ◽  
Gonadal Development ◽  
Male Gonad ◽  
Hub Gene ◽  
Gonad Differentiation ◽  
Genetic Mechanisms ◽  
And Function ◽  
Bipotential Gonad ◽  
Sox9 Protein

Sex determination occurs early during embryogenesis among vertebrates. It involves the differentiation of the bipotential gonad to ovaries or testes by a fascinating diversity of molecular switches. In most mammals, the switch is SRY (sex determining region Y); in other vertebrates it could be one of a variety of genes including Dmrt1 or dmy. Downstream of the switch gene, SOX9 upregulation is a central event in testes development, controlled by gonad-specific enhancers across the 2 Mb SOX9 locus. SOX9 is a ‘hub’ gene of gonadal development, regulated positively in males and negatively in females. Despite this diversity, SOX9 protein sequence and function among vertebrates remains highly conserved. This article explores the cellular, morphological, and genetic mechanisms initiated by SOX9 for male gonad differentiation.

Sex Reversal and Analyses of Possible Involvement of Sex Steroids in Scallop Gonadal Development in Newly Established Organ-Culture Systems

2017 ◽  
Vol 34 (2) ◽  
pp. 86 ◽  
Author(s):  
Ayano Otani ◽  
Tadaaki Nakajima ◽  
Tomomi Okumura ◽  
Shiro Fujii ◽  
Yasuhiro Tomooka
Keyword(s):  
Organ Culture ◽  
Sex Steroids ◽  
Gonadal Development ◽  
Sex Reversal ◽  
Culture Systems

scholarly journals Inheritance of T-associated sex reversal in mice

1990 ◽  
Vol 56 (2-3) ◽  
pp. 185-191 ◽  
Author(s):  
Linda L. Washburn ◽  
Barbara K. Lee ◽  
Eva M. Eicher
Keyword(s):  
Sex Determination ◽  
Inbred Strain ◽  
Y Chromosome ◽  
Ovarian Tissue ◽  
Testicular Tissue ◽  
Gonadal Development ◽  
Sex Reversal ◽  
Testicular Development ◽  
Additional Locus ◽  
Strain Background

SummaryWe previously identified a primary sex-determining locus,Tas, on mouse Chr 17 that causes ovarian tissue development in C57BL/6JThp/ + andTorl/ + individuals if the AKR/J Y chromosome is present. We hypothesized thatTasis located within the region of Chr 17 deleted byThpandTorland that C57BL/6J carries a diagnosticTasallele, based on the observation that ovarian tissue develops in XY mice whenThpis on a C57BL/6J inbred strain background, whereas normal testicular development occurs whenThpis on a C3H/HeSnJ inbred strain background. To test this hypothesis, we mated (C57BL/6J × C3H/HeSnJ)F1 females to C57BL/6JThp/ + hermaphrodites. As expected, half of the XYThp/+ offspring developed ovarian and testicular tissue while half developed exclusively testicular tissue. Unexpectedly, the inheritance of selected Chr 17 molecular loci was independent of gonadal development, as half of the male and hermaphroditic offspring inherited C3H/HeSnJ-derived Chr 17 loci and half inherited C57BL/6J-derived Chr 17 loci. We conclude that for ovarian tissue to develop in an XYThp/ + or XYTort/ + individual (1)Tasmust be present in a hemizygous state, which is accomplished by heterozygosity for theThporTortdeletions; (2) the AKR/J-derived Y chromosome must be present; and (3) an additional locus involved in primary sex determination must be present in a homozygous C57BL/6J state. This newly identified gene may be one of the previously defined loci,tda-1ortda-2.

scholarly journals Expression of steroidogenic factor 1 and Wilms' tumour 1 during early human gonadal development and sex determination

1999 ◽  
Vol 87 (1-2) ◽  
pp. 175-180 ◽  
Author(s):  
N.A. Hanley ◽  
S.G. Ball ◽  
M. Clement-Jones ◽  
D.M. Hagan ◽  
T. Strachan ◽  
...  
Keyword(s):  
Sex Determination ◽  
Gonadal Development ◽  
Wilms Tumour ◽  
Steroidogenic Factor 1 ◽  
Early Human

scholarly journals Sex Ratios in a Warming World: Thermal Effects on Sex-Biased Survival, Sex Determination, and Sex Reversal

2021 ◽  
Vol 112 (2) ◽  
pp. 155-164
Author(s):  
Suzanne Edmands
Keyword(s):  
High Temperature ◽  
Sex Ratio ◽  
Sex Determination ◽  
Heat Tolerance ◽  
Sex Ratios ◽  
Sex Reversal ◽  
Survival Sex ◽  
Ratio Distortion ◽  
Warming World ◽  
Sex Ratio Distortion

Abstract Rising global temperatures threaten to disrupt population sex ratios, which can in turn cause mate shortages, reduce population growth and adaptive potential, and increase extinction risk, particularly when ratios are male biased. Sex ratio distortion can then have cascading effects across other species and even ecosystems. Our understanding of the problem is limited by how often studies measure temperature effects in both sexes. To address this, the current review surveyed 194 published studies of heat tolerance, finding that the majority did not even mention the sex of the individuals used, with <10% reporting results for males and females separately. Although the data are incomplete, this review assessed phylogenetic patterns of thermally induced sex ratio bias for 3 different mechanisms: sex-biased heat tolerance, temperature-dependent sex determination (TSD), and temperature-induced sex reversal. For sex-biased heat tolerance, documented examples span a large taxonomic range including arthropods, chordates, protists, and plants. Here, superior heat tolerance is more common in females than males, but the direction of tolerance appears to be phylogenetically fluid, perhaps due to the large number of contributing factors. For TSD, well-documented examples are limited to reptiles, where high temperature usually favors females, and fishes, where high temperature consistently favors males. For temperature-induced sex reversal, unambiguous cases are again limited to vertebrates, and high temperature usually favors males in fishes and amphibians, with mixed effects in reptiles. There is urgent need for further work on the full taxonomic extent of temperature-induced sex ratio distortion, including joint effects of the multiple contributing mechanisms.

Roles of Anti-Müllerian hormone (Amh) and its duplicates in sex determination and germ cell proliferation of Nile tilapia

Genetics ◽  
2021 ◽  
Author(s):  
Xingyong Liu ◽  
Shengfei Dai ◽  
Jiahong Wu ◽  
Xueyan Wei ◽  
Xin Zhou ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Sex Determination ◽  
Germ Cell ◽  
Y Chromosome ◽  
X Chromosome ◽  
Nile Tilapia ◽  
Critical Period ◽  
Sex Reversal ◽  
Homozygous Mutation ◽  
Germ Cell Proliferation

Abstract Duplicates of amh are crucial for fish sex determination and differentiation. In Nile tilapia, unlike in other teleosts, amh is located on X chromosome. The Y chromosome amh (amh△-y) is mutated with 5 bp insertion and 233 bp deletion in the coding sequence, and tandem duplicate of amh on Y chromosome (amhy) has been identified as the sex determiner. However, the expression of amh, amh△-y and amhy, their roles in germ cell proliferation and the molecular mechanism of how amhy determines sex is still unclear. In this study, expression and functions of each duplicate were analyzed. Sex reversal occurred only when amhy was mutated as revealed by single, double and triple mutation of the three duplicates in XY fish. Homozygous mutation of amhy in YY fish also resulted in sex reversal. Earlier and higher expression of amhy/Amhy was observed in XY gonads compared with amh/Amh during sex determination. Amhy could inhibit the transcription of cyp19a1a through Amhr2/Smads signaling. Loss of cyp19a1a rescued the sex reversal phenotype in XY fish with amhy mutation. Interestingly, mutation of both amh and amhy in XY fish or homozygous mutation of amhy in YY fish resulted in infertile females with significantly increased germ cell proliferation. Taken together, these results indicated that up-regulation of amhy during the critical period of sex determination makes it the sex-determining gene, and it functions through repressing cyp19a1a expression via Amhr2/Smads signaling pathway. Amh retained its function in controlling germ cell proliferation as reported in other teleosts, while amh△-y was nonfunctionalized.

Sex steroids regulate pro- and anti-inflammatory cytokine release by macrophages after trauma-hemorrhage

1999 ◽  
Vol 277 (1) ◽  
pp. C35-C42 ◽  
Author(s):  
Martin K. Angele ◽  
Markus W. Knöferl ◽  
Martin G. Schwacha ◽  
Alfred Ayala ◽  
William G. Cioffi ◽  
...  
Keyword(s):  
Immune Responses ◽  
Peritoneal Macrophage ◽  
Kupffer Cell ◽  
Sex Steroids ◽  
Sham Operation ◽  
Male And Female ◽  
Splenic Macrophage ◽  
Female Sex ◽  
17Β Estradiol ◽  
Tissue Trauma

Studies indicate that macrophage immune responses in males are depressed after trauma-hemorrhage, whereas they are enhanced in females under such conditions. Nonetheless, the involvement of male and female sex steroids in this gender-dependent dimorphic immune response after trauma-hemorrhage remains unclear. To study this, male C3H/HeN mice were castrated and treated with pellets containing either vehicle, 5α-dihydrotestosterone (DHT), 17β-estradiol, or a combination of both steroid hormones for 14 days before soft tissue trauma (i.e., laparotomy) and hemorrhagic shock (35 ± 5 mmHg for 90 min followed by adequate fluid resuscitation) or a sham operation. Twenty-four hours later the animals were killed, plasma was obtained, and Kupffer cell and splenic and peritoneal macrophage cultures were established. For DHT-treated mice, we observed significantly decreased releases of the proinflammatory cytokines interleukin 1β (IL-1β) and IL-6 by splenic macrophage (−50 and −57%, respectively) and peritoneal macrophage (−51 and −52%, respectively) cultures after trauma-hemorrhage compared with releases by cultures of cells from mice subjected to a sham operation; in contrast, responses of splenic and peritoneal macrophage cultures from other groups subjected to trauma-hemorrhage did not change significantly. In addition, only DHT-treated animals exhibited increased Kupffer cell IL-6 release (+634%). The release of IL-10 in DHT-treated hemorrhaged animals was increased compared with that in sham-operated animals but was decreased in estrogen-treated mice under such conditions. These results suggest that male and female sex steroids exhibit divergent immunomodulatory properties with respect to cell-mediated immune responses after trauma-hemorrhage.

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