Genes Regulating Testis Size1

Chubb, Curtis

doi:10.1095/biolreprod47.1.29

Cited by 36 publications

(29 citation statements)

References 25 publications

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“…Sertoli cell number is the primary determinant of mature testicular size and capacity to produce sperm (Orth et al 1988, Russell et al 1990, Chubb 1992, and thus therein resides potential to decrease production (artificial E. *P,0·05; **P,0·01; ***P,0·001; dpc, days postcoitum; dpp, days postpartum; Brd, Breed; NS, not significant.…”

Section: Discussionmentioning

confidence: 99%

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Stereological evaluation of Sertoli cell ontogeny during fetal and neonatal life in two diverse breeds of swine

McCoard¹,

Wise²,

Lunstra³

et al. 2003

Journal of Endocrinology

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Chinese Meishan (MS) boars have smaller testes due to fewer Sertoli cells compared with White Composite (WC) boars. The objective was to describe Sertoli cell development relative to circulating FSH concentrations in fetal and neonatal MS and WC boars. Testes and blood samples were collected on days 60, 75, 90 and 105 postcoitum (dpc) and 1, 7, 14 and 25 postpartum (dpp). One testis was immunostained for GATA4 or Ki67 antigen to evaluate total and proliferating Sertoli cell numbers respectively. Testicular size was greater (P,0·01) in WC than MS boars at all ages, associated with a greater mass of interstitial tissue. Tubular mass (P,0·01) was greater in prenatal WC boars, but postnatally increased more rapidly (P,0·001) in MS boars, exceeding WC boars by 25 dpp. Sertoli cell numbers increased with age, was greater (P,0·001) in WC than MS boars during prenatal development but increased rapidly (P,0·01) by 1 dpp in MS and thereafter was similar in both breeds. The proportion of Ki67-positive Sertoli cells was maximal at 90 dpc, declining thereafter, did not differ between breeds through 7 dpp, but was greater (P,0·05) in WC than MS boars at 14 and 25 dpp. Plasma FSH concentrations were greater (P,0·05) in WC than MS boars at 75 dpc. FSH concentrations were elevated at 105 dpc (MS) and 1 dpp (WC) but declined thereafter with advancing postnatal age in both breeds. This study illustrates that late gestation represents the period of maximal Sertoli cell proliferation. Despite asynchronous Sertoli cell population growth between breeds during early postnatal life, differential mature Sertoli cell numbers and testicular size are probably due to differences in duration of the proliferative period after 25 dpp, potentially regulated by Sertoli cell maturation and blood-testis barrier formation. These events were not associated with fetal or early postnatal changes in FSH secretion.

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Section: Discussionmentioning

confidence: 99%

“…Sertoli cell numbers determine adult testicular size (Orth 1984, Russell et al 1990, Chubb 1992, thereby establishing an upper limit for total daily sperm production. Thus boars with large testes provide an opportunity to decrease production costs for artificial insemination while simultaneously allowing use of genetically superior sires.…”

Section: Introductionmentioning

confidence: 99%

Stereological evaluation of Sertoli cell ontogeny during fetal and neonatal life in two diverse breeds of swine

McCoard¹,

Wise²,

Lunstra³

et al. 2003

Journal of Endocrinology

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“…A reduction in testicular size may be a reflection of the reduction in the number of germ cells within the seminiferous tubules (25). To investigate this, P0.5 testis sections were immunostained for the mouse vasa homolog (MVH; Fig.…”

Section: Aspm Mutations Cause Major Defects In the Male And Femalementioning

confidence: 99%

Mutations in mouse Aspm (abnormal spindle-like microcephaly associated) cause not only microcephaly but also major defects in the germline

Pulvers

Bryk

Fish

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

182

187

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Mutations in ASPM (abnormal spindle-like microcephaly associated) cause primary microcephaly in humans, a disorder characterized by a major reduction in brain size in the apparent absence of nonneurological anomalies. The function of the Aspm protein in neural progenitor cell expansion, as well as its localization to the mitotic spindle and midbody, suggest that it regulates brain development by a cell division-related mechanism. Furthermore, evidence that positive selection affected ASPM during primate evolution has led to suggestions that such a function changed during primate evolution. Here, we report that in Aspm mutant mice, truncated Aspm proteins similar to those causing microcephaly in humans fail to localize to the midbody during M-phase and cause mild microcephaly. A human ASPM transgene rescues this phenotype but, interestingly, does not cause a gain of function. Strikingly, truncated Aspm proteins also cause a massive loss of germ cells, resulting in a severe reduction in testis and ovary size accompanied by reduced fertility. These germline effects, too, are fully rescued by the human ASPM transgene, indicating that ASPM is functionally similar in mice and humans. Our findings broaden the spectrum of phenotypic effects of ASPM mutations and raise the possibility that positive selection of ASPM during primate evolution reflects its function in the germline.evolution | cerebral cortex | fertility | neural stem cells | germ cells

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“…Studies in strains of mice which differ in the testis size lead to the conclusion that testis size is under the control of at least two autosomal genes which exert their effect by regulating the number of Sertoli cells (Chubb, 1992).…”

Section: 6mentioning

confidence: 99%

Return of testicular function after vaccination of boars against GnRH: consequences on testes histology

Rottner

Claus

2009

Animal

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Traditionally, male pigs are surgically castrated without anaesthesia to avoid later occurrence of the sex odour of androstenone in the carcass. Active immunization against gonadotropin-releasing hormone (GnRH) is a painless alternative which inhibits LH and thus steroidogenesis in the Leydig cells. In a preceding study we clarified the return of Leydig cell function after the last dose of antigen by measuring hormones, and found a considerable variation (10 to 24 weeks) till return of their function (testosterone > 0.5 ng/ml blood plasma). The present paper analyses histological data on testes characteristics of the same six boars at an age of 52 weeks (26 weeks after last immunization). Data were compared to another four boars which were not immunized but slaughtered at the same age. Testis weight was related to the concentration of testosterone in blood. In boars, that first returned to testicular function, testis weight even exceeded those in controls probably due to rebound phenomena. Differences in testis weight were mainly due to differences of Leydig cell content of cytoplasm, and less to the size of nuclei. Additionally, the height of seminiferous epithelium was slightly dependent on testosterone concentrations and contributed moderately to differences in testis weight. Altogether, normalization of testicular function, even after return to steroidogenesis, requires another 13 weeks.

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Genes Regulating Testis Size1

Cited by 36 publications

References 25 publications

Stereological evaluation of Sertoli cell ontogeny during fetal and neonatal life in two diverse breeds of swine

Stereological evaluation of Sertoli cell ontogeny during fetal and neonatal life in two diverse breeds of swine

Mutations in mouse Aspm (abnormal spindle-like microcephaly associated) cause not only microcephaly but also major defects in the germline

Return of testicular function after vaccination of boars against GnRH: consequences on testes histology

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