scholarly journals Connection between seminiferous tubules and epididymal duct is originally induced before sex differentiation in a sex‐independent manner

2020 ◽  
Vol 249 (6) ◽  
pp. 754-764 ◽  
Author(s):  
Takuya Omotehara ◽  
Xi Wu ◽  
Miyuki Kuramasu ◽  
Masahiro Itoh
Development ◽  
1964 ◽  
Vol 12 (2) ◽  
pp. 289-308
Author(s):  
L. L. Franchi ◽  
Anita M. Mandl

The Gonads of the rat undergo sex differentiation on the 14th day post coitum (p.c.), the testis becoming clearly distinguishable by the presence of an incipient tunica albuginea. The male germ cells become incorporated into medullary cords (the precursors of seminiferous tubules). In contrast, the germ cells in ovaries are scattered in cortical nests. Recent quantitative studies have shown that at 14·5 days p.c., the number of germ cells is somewhat greater in the male than the female (Beaumont & Mandl, 1963; cf. Beaumont & Mandl, 1962). In both sexes mitotic activity ceases at about 18·5 days p.c. Thereafter, the male germ cells remain at prolonged interphase; a proportion of them show histological changes frequently associated with degeneration. Quantitative estimates, on the other hand, indicate that none are eliminated from the testis. In the coeval female, the germ cells enter the prophase of meiosis, whereafter no further mitotic divisions are possible.


2013 ◽  
Vol 14 (S1) ◽  
Author(s):  
Andrea Mietens ◽  
Gerrit Eichner ◽  
Sabine Tasch ◽  
Caroline Feuerstacke ◽  
Ingrid Schneider-Hüther ◽  
...  

2021 ◽  
Vol 118 (23) ◽  
pp. e2024067118
Author(s):  
Daiki Kajioka ◽  
Kentaro Suzuki ◽  
Shoko Matsushita ◽  
Shinjiro Hino ◽  
Tetsuya Sato ◽  
...  

Testicular androgen is a master endocrine factor in the establishment of external genital sex differences. The degree of androgenic exposure during development is well known to determine the fate of external genitalia on a spectrum of female- to male-specific phenotypes. However, the mechanisms of androgenic regulation underlying sex differentiation are poorly defined. Here, we show that the genomic environment for the expression of male-biased genes is conserved to acquire androgen responsiveness in both sexes. Histone H3 at lysine 27 acetylation (H3K27ac) and H3K4 monomethylation (H3K4me1) are enriched at the enhancer of male-biased genes in an androgen-independent manner. Specificity protein 1 (Sp1), acting as a collaborative transcription factor of androgen receptor, regulates H3K27ac enrichment to establish conserved transcriptional competency for male-biased genes in both sexes. Genetic manipulation of MafB, a key regulator of male-specific differentiation, and Sp1 regulatory MafB enhancer elements disrupts male-type urethral differentiation. Altogether, these findings demonstrate conservation of androgen responsiveness in both sexes, providing insights into the regulatory mechanisms underlying sexual fate during external genitalia development.


PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5094 ◽  
Author(s):  
Luzie Jessl ◽  
Rebecca Lenz ◽  
Fabian G. Massing ◽  
Jessica Scheider ◽  
Jörg Oehlmann

Since it is known that environmental contaminants have the potential to cause endocrine disorders in humans and animals, there is an urgent need for in vivo tests to assess possible effects of these endocrine disrupting chemicals (EDCs). Although there is no standardized guideline, the avian embryo has proven to be particularly promising as it responds sensitively to a number of EDCs preferentially impacting the reproductive axis. In the present study we examined the effects of in ovo exposure to fulvestrant and tamoxifen as antiestrogenic model compounds and co-exposure to both substances and the potent estrogen 17α-ethinylestradiol (EE2) regarding sex differentiation and embryonic development of the domestic fowl (Gallus gallus domesticus). The substances were injected into the yolk of fertilized eggs on embryonic day 1. On embryonic day 19 sex genotype and phenotype were determined, followed by gross morphological and histological examination of the gonads. Sole EE2-treatment (20 ng/g egg) particularly affected male gonads and resulted in an increased formation of female-like gonadal cortex tissue and a reduction of seminiferous tubules. In ovo exposure to tamoxifen (0.1/1/10 µg/g egg) strongly impaired the differentiation of female gonads, led to a significant size reduction of the left ovary and induced malformations of the ovarian cortex, while fulvestrant (0.1/1/10 µg/g egg) did not affect sexual differentiation. However, both antiestrogens were able to antagonize the feminizing effects of EE2in genetic males when administered simultaneously. Since both estrogens and antiestrogens induce concentration-dependent morphological alterations of the sex organs, the chick embryo can be regarded as a promising model for the identification of chemicals with estrogenic and antiestrogenic activity.


1992 ◽  
Vol 28 (4) ◽  
pp. 527
Author(s):  
Myung Seob Lee ◽  
Myung Soon Kim ◽  
Hyun Ju Park

2019 ◽  
Vol 1 (1) ◽  
pp. 1-5
Author(s):  
Abyt Ibraimov

In many animals, including us, the genetic sex is determined at fertilization by sex chromosomes. Seemingly, the sex determination (SD) in human and animals is determined by the amount of constitutive heterochromatin on Y chromosome via cell thermoregulation. It is assumed the medulla and cortex tissue cells in the undifferentiated embryonic gonads (UEG) differ in vulnerability to the increase of the intracellular temperature. If the amount of the Y chromosome constitutive heterochromatin is enough for efficient elimination of heat difference between the nucleus and cytoplasm in rapidly growing UEG cells the medulla tissue survives. Otherwise it doomed to degeneration and a cortex tissue will remain in the UEG. Regardless of whether our assumption is true or not, it remains an open question why on Y chromosome there is a large constitutive heterochromatin block? What is its biological meaning? Does it relate to sex determination, sex differentiation and development of secondary sexual characteristics? If so, what is its mechanism: chemical or physical? There is no scientifically sound answer to these questions.


Reproduction ◽  
2000 ◽  
pp. 443-452 ◽  
Author(s):  
MA Peters ◽  
DG de Rooij ◽  
KJ Teerds ◽  
I van Der Gaag ◽  
FJ van Sluijs

Spermatogenesis was examined in testes from 74 dogs of various breeds without clinically detected testicular disease. A modified Johnsen score system was used to determine whether spermatogenesis deteriorates with ageing. The diameter of seminiferous tubules was measured in dogs without testicular disease to examine other possible effects of ageing on tubular performance. There appeared to be no relation between age and these variables. The influence of testicular tumours on spermatogenesis was also investigated in both affected and unaffected testes. The testes of 28 dogs with clinically palpable tumours and 21 dogs with clinically non-palpable tumours were investigated. In cases of unilateral occurrence of a tumour, impairment of spermatogenesis was observed only in the affected testis of dogs with clinically detected tumours. Bilateral occurrence of tumours, whether detected clinically or non-clinically, was associated with severe impairment of spermatogenesis. The prevalence of tumours increased during ageing. Eighty-six per cent of the clinically detected and 57% of the non-clinically detected tumours were found in old dogs. Multiple types of tumour and bilateral occurrence were very common. Seminomas and Leydig cell tumours were more frequent than Sertoli cell tumours. It was concluded that spermatogenesis per se did not decrease during ageing in dogs but the occurrence of testicular tumours increased with ageing and affected spermatogenesis significantly, as reflected by a lower Johnsen score.


Reproduction ◽  
2000 ◽  
pp. 325-335 ◽  
Author(s):  
A Calvo ◽  
LM Pastor ◽  
S Bonet ◽  
E Pinart ◽  
M Ventura

Lectin histochemistry was used to perform in situ characterization of the glycoconjugates present in boar testis and epididymis. Thirteen horseradish peroxidase- or digoxigenin-labelled lectins were used in samples obtained from healthy fertile boars. The acrosomes of the spermatids were stained intensely by lectins with affinity for galactose and N-acetyl-galactosamine residues, these being soybean, peanut and Ricinus communis agglutinins. Sertoli cells were stained selectively by Maackia ammurensis agglutinin. The lamina propria of seminiferous tubules showed the most intense staining with fucose-binding lectins. The Golgi area and the apical part of the principal cells of the epididymis were stained intensely with many lectins and their distribution was similar in the three zones of the epididymis. On the basis of lectin affinity, both testis and epididymis appear to have N- and O-linked glycoconjugates. Spermatozoa from different epididymal regions showed different expression of terminal galactose and N-acetyl-galactosamine. Sialic acid (specifically alpha2,3 neuraminic-5 acid) was probably incorporated into spermatozoa along the extratesticular ducts. These findings indicate that the development and maturation of boar spermatozoa are accompanied by changes in glycoconjugates. As some lectins stain cellular or extracellular compartments specifically, these lectins could be useful markers in histopathological evaluation of diseases of boar testis and epididymis.


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