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Induction of apoptosis involving multiple pathways is a primary response to cyclin A1‐deficiency in male meiosis
Author(s) -
Salazar Glicella,
Joshi Ayesha,
Liu Dong,
Wei Hongquan,
Persson Jenny Liao,
Wolgemuth Debra J.
Publication year - 2005
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20533
Subject(s) - biology , spermatogenesis , apoptosis , tunel assay , spermatocyte , cyclin b1 , cyclin , cyclin d1 , microbiology and biotechnology , meiosis , germ cell , cell cycle , andrology , gene , genetics , endocrinology , cyclin dependent kinase 1 , medicine
The meiotic arrest in male mice null for the cyclin A1 gene ( Ccna1 ) was associated with apoptosis of spermatocytes. To determine whether the apoptosis in spermatocytes was triggered in response to the arrest at G2/M phase, as opposed to being a secondary response to overall disruption of spermatogenesis, we examined testes during the first wave of spermatogenesis by terminal deoxynucleotidyl transferase–mediated deoxyuridinetriphosphate nick end‐labeling (TUNEL) staining. We observed enhanced apoptosis coinciding with the arrest point in postnatal day 22 tubules, with no overt degeneration. Along with activation of caspase‐3, an increase in the levels and change of subcellular localization of Bax protein was observed in cyclin A1–deficient spermatocytes, which coincided with the detection of apoptosis. As p53 is implicated in the activation of Bax‐mediated cell death, we generated mice lacking both cyclin A1 and p53. Although the absence of p53 did not rescue the meiotic arrest, there was a decrease in the number of apoptotic cells in the double‐mutant testes. This finding suggested that p53 may be involved in the process by which the arrested germ cells are removed from the seminiferous tubules but that other pathways function as well to ensure removal of the arrested spermatocytes. Developmental Dynamics 234:114–123, 2005. © 2005 Wiley‐Liss, Inc.