Document Detail

p53-dependent apoptosis in the inhibition of spermatogonial differentiation in juvenile spermatogonial depletion (Utp14bjsd) mice.
MedLine Citation:
PMID:  18356279     Owner:  NLM     Status:  MEDLINE    
In adult male mice homozygous for the juvenile spermatogonial depletion (Utp14b jsd) mutation in the Utp14b gene, type A spermatogonia proliferate, but in the presence of testosterone and at scrotal temperatures, these spermatogonia undergo apoptosis just before differentiation. In an attempt to delineate this apoptotic pathway in jsd mice and specifically address the roles of p53- and Fas ligand (FasL) /Fas receptor-mediated apoptosis, we produced jsd mice deficient in p53, Fas, or FasL. Already at the age of 5 wk, less degeneration of spermatogenesis was observed in p53-null-jsd mice than jsd single mutants, and in 8- or 12-wk-old mice, the percentage of seminiferous tubules showing differentiated germ cells [tubule differentiation index (TDI)] was 26-29% in the p53-null-jsd mice, compared with 2-4% in jsd mutants with normal p53. The TDI in jsd mice heterozygous for p53 showed an intermediate TDI of 8-13%. The increase in the differentiated tubules in double-mutant and p53 heterozygous jsd mice was mostly attributable to intermediate and type B spermatogonia; few spermatocytes were present. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling staining showed that most of these differentiated spermatogonia still underwent apoptosis, thereby blocking further continuation of spermatogenesis. In contrast, the percentage of tubules that were differentiated was not significantly altered in either adult Fas null-jsd mice or adult FasL defective gld-jsd double mutant mice as compared with jsd single mutants. Furthermore, caspase-9, but not caspase-8 was immunochemically localized in the adult jsd mice spermatogonia undergoing apoptosis. The results show that p53, but not FasL or Fas, is involved in the apoptosis of type A spermatogonia before/during differentiation in jsd mice that involves the intrinsic pathway of apoptosis. However, apoptosis in the later stages must be a p53-independent process.
Gunapala Shetty; Shan H Shao; Connie C Y Weng
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2008-03-20
Journal Detail:
Title:  Endocrinology     Volume:  149     ISSN:  0013-7227     ISO Abbreviation:  Endocrinology     Publication Date:  2008 Jun 
Date Detail:
Created Date:  2008-05-21     Completed Date:  2008-08-08     Revised Date:  2013-03-27    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2773-81     Citation Subset:  AIM; IM    
Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
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MeSH Terms
Antigens, CD95 / genetics
Cryptorchidism / pathology
Fas Ligand Protein / genetics
Germ Cells / cytology,  physiology
In Situ Nick-End Labeling
Mice, Knockout
Ribonucleoproteins, Small Nucleolar / deficiency,  genetics*
Spermatogonia / cytology*,  physiology
Testis / cytology,  physiology
Tumor Suppressor Protein p53 / genetics*
Grant Support
Reg. No./Substance:
0/Antigens, CD95; 0/Fas Ligand Protein; 0/Ribonucleoproteins, Small Nucleolar; 0/Tumor Suppressor Protein p53; 0/Utp14b protein, mouse

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