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Home CCSU Theses & Dissertations IS mshi/mshi STERILITY THE RESULT OF CASPASE-3-MEDIATED APOPTOSIS OF SPERMATOGONIA AT PUBERTY?

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IS mshi/mshi STERILITY THE RESULT OF CASPASE-3-MEDIATED APOPTOSIS OF SPERMATOGONIA AT PUBERTY?

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Identifier	Thesis 1754
Author	Compton, Tiwanna
Title	IS mshi/mshi STERILITY THE RESULT OF CASPASE-3-MEDIATED APOPTOSIS OF SPERMATOGONIA AT PUBERTY?
Publisher	Central Connecticut State University
Date	2004
Resource Type	Master's Thesis
Notes	The autosomal recessive mshi mutation in BALB/cBy mice phenotypically causes reduced testis size and male sterility in homozygotes. The development of the mshi male generative organs, prior to three weeks of age, appears to lack observable abnormalities, but by three to four weeks post-partum, testicular deformity in mshi/mshi mice is detected histologically (Myrie, 1997). The sudden loss of virtually all spermatocytes in these mice suggests that type A spermatogonia inappropriately elect to undergo apoptosis at puberty rather than proceed with the spermatogenic process. To determine whether apoptosis is occurring in the testes of mshi/mshi pubescent males, the CaspACE Assay System, Colorimetric (Promega Corporation, Madison, Wisconsin) was used in this study to measure the activity of caspase-3 (a caspase that plays a vital role in many apoptotic pathways) in both mutant and heterozygous control testes. Throughout the period of this study, caspase-3 displayed similar activity in the mutant and heterozygous control testes, suggesting that if apoptosis is the cause of spermatogonial reduction in mutant testes at puberty, a signalling pathway that does not involve caspase-3 must mediate it. The testicular weights of the controls were approximately three times larger than the testicular weights of the mutants at seven weeks of age. No substantial change in the weights of the mutant testes was seen after four weeks, but the weights of the wild type and heterozygous control testes greatly increased. There was no substantial change in caspase-3 activity between weeks 4 and 5 or between the mutants and the controls. An abnormality somehow hindered the increase of the mutant testes weight, and the data suggest that the abnormality was independent of caspase-3. Thus, caspase-3 activity does not appear to be involved in the inappropriate loss of the mutant spermatogonia because the mutants and the controls have very similar levels of activity at all ages tested. However, if all the caspase-3 activity is from germ cells, which after 3 weeks the mutants and controls have vastly different amounts, increased caspase-3 activity might be related to the mutant phenotype.
Subject	Mice -- Anatomy Mice -- Development
Department	Department of Biological Sciences
Advisor	Mulrooney, James P
Type	Text
Digital Format	application/pdf
Language	eng
OCLC number	713733902
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IS mshi/mshi STERILITY THE RESULT OF CASPASE-3-MEDIATED APOPTOSIS OF SPERMATOGONIA AT PUBERTY?

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