Which statement about spermatogenesis is correct

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Instant Video Solutions. Request OTP. Updated On: However, based on the results from meta-analyses — caution is needed with the use of FSH, especially as it relates to high dosage and long-term treatments. In addition, more carefully controlled studies should be carried out to identify individuals with possible specific genetic makeup, who would most likely benefit from FSH treatment. All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The mammalian blood-testis barrier: its biology and regulation. Endocr Rev. Steinberger E, Steinberger A. Spermatogenic function of the testis. Handbook of Physiology. Google Scholar. Griswold MD. The central role of Sertoli cells in spermatogenesis. Semin Cell Dev Biol. Sharpe RM.

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Eur J Med Genet. An activated human follicle-stimulating hormone FSH receptor stimulates FSH-like activity in gonadotropin-deficient transgenic mice. Mol Endocrinol. Neonatal exposure of rats to recombinant follicle stimulating hormone increases adult Sertoli and spermatogenic cell numbers. Biol Reprod. Constitutively active follicle-stimulating hormone receptor enables androgen-independent spermatogenesis. J Clin Invest.

Testicular development in mice lacking receptors for follicle stimulating hormone and androgen. Clermont Y, Perey B. Quantitative study of the cell population of the seminiferous tubules in immature rats. Am J Anat. Use of in vitro systems to study male germ cell development in neonatal rats. Theriogenology —9. Stage-specific expression of the FSH receptor gene in the prepubertal and adult rat seminiferous epithelium.

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FSH immunoneutralization acutely impairs spermatogonial development in normal adult rats. Mol Hum Reprod. Preferential beta-arrestin signalling at low receptor density revealed by functional characterization of the human FSH receptor A V mutation. Analysis of protein-coding genetic variation in 60, humans. Nature — Male hypogonadism resulting from mutations in the genes for gonadotropin subunits and their receptors.

In: Winters S, Huhtaniemi I, editors. Gonadotroph adenomas in men produce biologically active follicle-stimulating hormone. Snyder PJ. Gonadotroph cell pituitary adenomas. Endocrinol Metab Clin North Am. Obstet Gynecol Surv. An activating mutation of the follicle-stimulating hormone receptor autonomously sustains spermatogenesis in a hypophysectomized man. Normal testicular function without detectable follicle-stimulating hormone. J Pediatr. Sexual precocity—genetic bases of central precocious puberty and autonomous gonadal activation.

Endocr Dev. Female mice expressing constitutively active mutants of FSH receptor present with a phenotype of premature follicle depletion and estrogen excess. Research resource: the dynamic transcriptional profile of sertoli cells during the progression of spermatogenesis. Oligonucleotide microarray analysis of gene expression in follicle-stimulating hormone-treated rat Sertoli cells. Follicle-stimulating hormone induced changes in gene expression of murine testis.

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Dev Biol. Reprogramming sertoli cells into pluripotent stem cells. Cell Reprogram — Atypical development of Sertoli cells and impairment of spermatogenesis in the hypogonadal hpg mouse. J Anat. Gene expression profiling of mouse Sertoli cell lines. Cell Tissue Res. FSH regulates the formation of adherens junctions and ectoplasmic specialisations between rat Sertoli cells in vitro and in vivo. In the male, estradiol only has a negative feedback effect on the levels of GnRH.

True False. GnRH binds to receptors on the surface of Leydig cells and via a calcium second messenger system, testosterone production and secretion is increased. In the bull, spermatogenesis involves the mitotic divisions of the sequence: Spermatogonium A to I to B and finally a primary spermatocyte. Meiosis is a part of spermatocytogenesis.

In the bull, there is the potential to produce 64 round spermatids from each type A spermatogonium that enters into spermatogenesis.

However this amount rarely occurs due to the natural process of apoptosis. Cytoplasmic bridges are a likely explanation for why protein expression on the surface of spermatozoa is not different between X and Y spermatozoa. Indentify which of the following will increase apoptosis in stallions. Going from April to November. Being exposed to trichamoniasis. Being kicked in the groin by a mare that was not in heat. Swelling did oocur from this incidence. An injection of testosterone.