Control of the annual testicular cycle of the marbled-newt by p53, p21, and Rb gene products
p53, p21, and Rb are proteins with an important role in cell‐cycle control. The expression and distribution of these gene products and the apoptotic rate were studied in the marbled‐newt testis along the annual cycle to know the role of these factors in the control of spermatogenesis and glandular t...
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Published in | Molecular reproduction and development Vol. 63; no. 2; pp. 202 - 209 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
New York
Wiley Subscription Services, Inc., A Wiley Company
01.10.2002
Wiley-Liss |
Subjects | |
Online Access | Get full text |
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Summary: | p53, p21, and Rb are proteins with an important role in cell‐cycle control. The expression and distribution of these gene products and the apoptotic rate were studied in the marbled‐newt testis along the annual cycle to know the role of these factors in the control of spermatogenesis and glandular tissue formation. The study was carried out using Western blot analysis and immunohistochemistry. The results differed from those, previously reported in mammals showing constant spermatogenesis. Greater expression of p53 and p21 was found in the quiescence period and was detected in PCGs (primordial germ cells), spermatogonia, follicular, interstitial cells, and glandular tissue. Greater expression of Rb and phosph‐Rb was present in the proliferation period, in PCGs, and spermatogonia. Apoptosis was only detected in secondary spermatogonia (quiescence and spermiogenesis periods) and primary spermatocytes (proliferation and spermiogenesis periods). In the quiescence period, the increase in p53 expression activates p21 expression, which inhibits Rb phosphorylation and arrests the cell cycle in G1. In the proliferation period and, in a lesser degree, in the spermiogenesis period, the expressions of p53 and p21 decrease and phosph‐Rb increases, enhancing cell proliferation. These gene products do not seem to be related to apoptosis Mol. Reprod. Dev. 63: 202–209, 2002. © 2002 Wiley‐Liss, Inc. |
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Bibliography: | ark:/67375/WNG-2PGBLJRT-C ArticleID:MRD10167 istex:67DBDD5113C345A3E2D1221B543F489544118EDF ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1040-452X 1098-2795 |
DOI: | 10.1002/mrd.10167 |