Role of mesonephric contribution to mouse testicular development revisited

2021 ◽  
Author(s):  
Gerald R. Cunha ◽  
Mei Cao ◽  
Sena Aksel ◽  
Amber Derpinghaus ◽  
Laurence S. Baskin

It has long been assumed that the mammalian Y chromosome either encodes, or controls the production of, a diffusible testis-determining molecule, exposure of the embryonic gonad to this molecule being all that is required to divert it along the testicular pathway. My recent finding that Sertoli cells in XX ↔ XY chimeric mouse testes are exclusively XY has led me to propose a new model in which the Y acts cell-autonomously to bring about Sertoli-cell differentiation. I have suggested that all other aspects of foetal testicular development are triggered by the Sertoli cells without further Y-chromosome involvement. This model thus equates mammalian sex determination with Sertoli-cell determination. Examples of natural and experimentally induced sex reversal are discussed in the context of this model.


2019 ◽  
Vol 34 (4) ◽  
pp. 339-348 ◽  
Author(s):  
Mahdiyeh Mirnamniha ◽  
Fereshteh Faroughi ◽  
Eisa Tahmasbpour ◽  
Pirooz Ebrahimi ◽  
Asghar Beigi Harchegani

Abstract Human semen contains several trace elements such as calcium (Ca), copper (Cu), manganese (Mn), magnesium (Mg), zinc (Zn) and selenium (Se) which are necessary for reproductive health, normal spermatogenesis, sperm maturation, motility and capacitation, as well as normal sperm function. In this review, the potential role of these trace elements in male reproductive health, normal function of spermatozoa and fertility potency were considered. We selected and reviewed articles that considered crucial roles of trace elements in human sperm function and fertility. Ca is essential for sperm motility and its hyperactivation, sperm capacitation and acrosome reaction, as well as sperm chemotaxis. Sodium (Na) and potassium (K) are involved in sperm motility and capacitation. Mg is necessary for normal ejaculation, spermatogenesis and sperm motility. Zn is one of the most significant nutrients in human semen. Seminal deficiency of Zn can be associated with delayed testicular development, impaired spermatogenesis, deficiency of sex hormones, oxidative stress and inflammation, and apoptosis. Se is another significant element which has antioxidative properties and is essential for spermatogenesis and the maintenance of male fertility. Mn is a potent stimulator for sperm motility; however, increased level of seminal plasma Se can be toxic for sperm. Like Se, Cu has antioxidative properties and has a positive effect on sperm parameters. Decreased level of these trace elements can negatively affect human reproductive health, semen quality, sperm normal function and as the result, fertility potency in men. Measurement of these trace elements in men with idiopathic infertility is necessary.


2007 ◽  
Vol 21 (3) ◽  
pp. 712-725 ◽  
Author(s):  
De-Shou Wang ◽  
Tohru Kobayashi ◽  
Lin-Yan Zhou ◽  
Bindhu Paul-Prasanth ◽  
Shigeho Ijiri ◽  
...  

Abstract Increasing evidence suggests the crucial role of estrogen in ovarian differentiation of nonmammalian vertebrates including fish. The present study has investigated the plausible role of Foxl2 in ovarian differentiation through transcriptional regulation of aromatase gene, using monosex fry of tilapia. Foxl2 expression is sexually dimorphic, like Cyp19a1, colocalizing with Cyp19a1 and Ad4BP/SF-1 in the stromal cells and interstitial cells in gonads of normal XX and sex-reversed XY fish, before the occurrence of morphological sex differentiation. Under in vitro conditions, Foxl2 binds to the sequence ACAAATA in the promoter region of the Cyp19a1 gene directly through its forkhead domain and activates the transcription of Cyp19a1 with its C terminus. Foxl2 can also interact through the forkhead domain with the ligand-binding domain of Ad4BP/SF-1 to form a heterodimer and enhance the Ad4BP/SF-1 mediated Cyp19a1 transcription. Disruption of endogenous Foxl2 in XX tilapia by overexpression of its dominant negative mutant (M3) induces varying degrees of testicular development with occasional sex reversal from ovary to testis. Such fish display reduced expression of Cyp19a1 as well as a drop in the serum levels of 17β-estradiol and 11-ketotestosterone. Although the XY fish with wild-type tilapia Foxl2 (tFoxl2) overexpression never exhibited a complete sex reversal, there were significant structural changes, such as tissue degeneration, somatic cell proliferation, and induction of aromatase, with increased serum levels of 17β-estradiol and 11-ketotestosterone. Altogether, these results suggest that Foxl2 plays a decisive role in the ovarian differentiation of the Nile tilapia by regulating aromatase expression and possibly the entire steroidogenic pathway.


2013 ◽  
Vol 137 (1-2) ◽  
pp. 74-81 ◽  
Author(s):  
R. Wells ◽  
A.L. Kenny ◽  
R. Duckett ◽  
N.G. Wreford ◽  
S.D. Johnston ◽  
...  

1999 ◽  
Vol 19 (3) ◽  
pp. 2289-2299 ◽  
Author(s):  
Jungho Kim ◽  
Dirk Prawitt ◽  
Nabeel Bardeesy ◽  
Elena Torban ◽  
Caroline Vicaner ◽  
...  

ABSTRACT Gonadal differentiation is dependent upon a molecular cascade responsible for ovarian or testicular development from the bipotential gonadal ridge. Genetic analysis has implicated a number of gene products essential for this process, which include Sry, WT1, SF-1, and DAX-1. We have sought to better define the role of WT1 in this process by identifying downstream targets of WT1 during normal gonadal development. We have noticed that in the developing murine gonadal ridge, wt1 expression precedes expression of Dax-1, a nuclear receptor gene. We document here that the spatial distribution profiles of both proteins in the developing gonad overlap. We also demonstrate that WT1 can activate the Dax-1 promoter. Footprinting analysis, transient transfections, promoter mutagenesis, and mobility shift assays suggest that WT1 regulates Dax-1via GC-rich binding sites found upstream of the Dax-1 TATA box. We show that two WT1-interacting proteins, the product of a Denys-Drash syndrome allele of wt1 and prostate apoptosis response-4 protein, inhibit WT1-mediated transactivation ofDax-1. In addition, we demonstrate that WT1 can activate the endogenous Dax-1 promoter. Our results indicate that the WT1–DAX-1 pathway is an early event in the process of mammalian sex determination.


1984 ◽  
Vol 12 (1) ◽  
pp. 49-51 ◽  
Author(s):  
A. Roy Chowdhury ◽  
U. Arora

2006 ◽  
Vol 13 (6) ◽  
pp. 785-793 ◽  
Author(s):  
YOSHIYUKI KOJIMA ◽  
SHOICHI SASAKI ◽  
YUTARO HAYASHI ◽  
YUKIHIRO UMEMOTO ◽  
KEN-ICHIRO MOROHASHI ◽  
...  

Author(s):  
M. García-García ◽  
M. Sánchez-Hernández ◽  
M.P. García-Hernández ◽  
A. García-Ayala ◽  
E. Chaves-Pozo

Reproduction ◽  
2005 ◽  
Vol 130 (5) ◽  
pp. 643-654 ◽  
Author(s):  
Helen Baines ◽  
Margaret O Nwagwu ◽  
Edwina C Furneaux ◽  
Jane Stewart ◽  
Jeffrey B Kerr ◽  
...  

Testicular development is arrested in the hypogonadal (hpg) mouse due to a congenital deficiency of hypothalamic gonadotropin-releasing hormone synthesis. Previous studies have demonstrated that chronic treatment of these mice with estradiol induces testicular maturation and qualitatively normal spermatogenesis, but it is not known whether these are direct effects via estrogen receptors expressed in the testis, or indirect actions via the pituitary gland. The aim of the current studies was to determine whether the actions of estradiol require the presence of androgens. Sensitive assays revealed that chronic estradiol treatment produced time-dependent increases in pituitary FSH production but no increases in pituitary LH or testicular testosterone content could be detected. As a functional test of androgen dependence, hpg mice were treated for 70 days with estradiol plus Casodex (bicalutamide), an androgen receptor antagonist. Casodex treatment markedly attenuated both the estradiol-induced increase in testicular weight and the proliferation of the seminiferous epithelium, as revealed by morphometric analysis. However, it did not affect the estradiol-induced increase in pituitary FSH content, nor did it affect estradiol-induced increases in the weight of the seminal vesicles and epididymides. We conclude that increased FSH production is not sufficient to explain the increase in testicular development induced by estradiol in hpg mice; there is a requirement for functional androgen receptors for induction of testicular growth.


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