Cell death patterns of the rat spermatogonial cell progeny induced by Sertoli cell geometric changes and Fas (CD95) agonist

Tres, Laura L.; Kierszenbaum, Abraham L.

doi:10.1002/(sici)1097-0177(199904)214:4<361::aid-aja8>3.0.co;2-x

Cited by 25 publications

(14 citation statements)

References 35 publications

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“…Intercellular bridges exist between differentiating spermatogenic cells, contributing to the synchronous development of germ cells derived from a single spermatogonium [38]. All daughter cells from a common spermatogonium can be selectively eliminated via apoptosis, whereas unrelated colonies are preserved [39]. The intercellular bridges allow macromolecules critical to the differentiation process to be shared among the daughter cells [40][41][42], which may share apoptotic signals within the colony.…”

Section: Discussionmentioning

confidence: 99%

BAX and Tumor Suppressor TRP53 Are Important in Regulating Mutagenesis in Spermatogenic Cells in Mice1

Vogel

McMahan

Herbert

et al. 2010

Biology of Reproduction

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During the first wave of spermatogenesis, and in response to ionizing radiation, elevated mutant frequencies are reduced to a low level by unidentified mechanisms. Apoptosis is occurring in the same time frame that the mutant frequency declines. We examined the role of apoptosis in regulating mutant frequency during spermatogenesis. Apoptosis and mutant frequencies were determined in spermatogenic cells obtained from Bax-null or Trp53-null mice. The results showed that spermatogenic lineage apoptosis was markedly decreased in Bax-null mice and was accompanied by a significantly increased spontaneous mutant frequency in seminiferous tubule cells compared to that of wild-type mice. Apoptosis profiles in the seminiferous tubules for Trp53-null were similar to control mice. Spontaneous mutant frequencies in pachytene spermatocytes and in round spermatids from Trp53-null mice were not significantly different from those of wild-type mice. However, epididymal spermatozoa from Trp53-null mice displayed a greater spontaneous mutant frequency compared to that from wild-type mice. A greater proportion of spontaneous transversions and a greater proportion of insertions/deletions 15 days after ionizing radiation were observed in Trp53-null mice compared to wild-type mice. Base excision repair activity in mixed germ cell nuclear extracts prepared from Trp53-null mice was significantly lower than that for wild-type controls. These data indicate that BAX-mediated apoptosis plays a significant role in regulating spontaneous mutagenesis in seminiferous tubule cells obtained from neonatal mice, whereas tumor suppressor TRP53 plays a significant role in regulating spontaneous mutagenesis between postmeiotic round spermatid and epididymal spermatozoon stages of spermiogenesis.

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Section: Discussionmentioning

confidence: 99%

BAX and Tumor Suppressor TRP53 Are Important in Regulating Mutagenesis in Spermatogenic Cells in Mice1

Vogel

McMahan

Herbert

et al. 2010

Biology of Reproduction

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“…The final concentration of the Fyn primer in the RT-PCR reactions was 160 nM. Sertolispermatogenic cell cocultures were prepared from 20-day-old rats as described previously (Tres and Kierszenbaum, 1999) and mRNA extracted after 2-4 days of coculture.…”

Section: Rt-pcr Analysismentioning

confidence: 99%

Expression of full‐length and truncated Fyn tyrosine kinase transcripts and encoded proteins during spermatogenesis and localization during acrosome biogenesis and fertilization

Kierszenbaum

Rivkin

Talmor-Cohen

et al. 2009

Molecular Reproduction Devel

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We report that full-length and truncated transcripts of Fyn tyrosine protein kinase are expressed during testicular development. Truncated Fyn (tr-Fyn) transcripts encode a 24 kDa protein with a N-terminal (NT) domain, a complete Src homology (SH) 3 domain and an incomplete SH2 domain. The kinase domain is missing in tr-Fyn. In contrast, full-length Fyn transcripts encode a 59-55 kDa protein. Fractionated spermatids by centrifugal elutriation express tr-Fyn transcripts and protein, but not full-length Fyn transcripts and protein. Neither full-length Fyn nor tr-Fyn transcripts and encoded proteins are detected in elutriated pachytene spermatocytes. Sertoli cells express full-length and truncated Fyn throughout testicular development. In contrast, sperm contain full-length Fyn transcripts and protein but not the truncated form. tr-Fyn protein is visualized at the cytosolic side of Golgi membranes, derived proacrosomal vesicles, along the outer acrosome membrane and the inner acrosome membrane-acroplaxome complex anchoring the acrosome to the spermatid nuclear envelope. Fyn and phosphotyrosine immunoreactivity coexist in the tail of capacitated sperm. During fertilization, the Fyn-containing acroplaxome seen in the egg-bound and egg-fused sperm is no longer detected upon decondensation of the sperm nucleus. tr-Fyn expands the catalog of truncated tyrosine protein kinases expressed during spermiogenesis. We suggest that the NT and SH3 domains of tr-Fyn may recruit adaptor and effector proteins, in particular GTPase activating proteins, required for acrosome-acroplaxome biogenesis, acroplaxome F-actin dynamics and Sertoli cell function. During fertilization, full-length Fyn in the acroplaxome may contribute to a transient local signaling burst during the early events of sperm-egg interaction.

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“…Therefore, we assume that in nonseasonal animals, Fas may be dispensable for germ cell degeneration during spermatogenesis. Although it was thought that Fas was not essential in germ cell homeostasis, recent reports still insist on the involvement of Fas in physiological death of germ cells (Wang et al, 1998;Tres and Kierszenbaum, 1999;Koji, 2001;Francavilla et al, 2002). It is well known that many small mammals stop breeding during the winter and their testes regress.…”

Section: (1) Fasmentioning

confidence: 99%

Physiological and Pathological Cell Deaths in the Reproductive Organs.

Sakamaki

2003

Cell Struct. Funct.

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Apoptosis of testicular germ cells and oocytes and their supporting cells in the gonads occurs at physiological and normal conditions or after exposure to pathological stimuli. Cell-death regulators, including Bcl-2 family members, caspases, Fas and p53 are thought to be involved in these processes. This article reviews the details of the apoptotic machinery in the reproductive organs by describing briefly the abnormal phenotypes observed in transgenic and gene-ablated mice.

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Cell death patterns of the rat spermatogonial cell progeny induced by Sertoli cell geometric changes and Fas (CD95) agonist

Cited by 25 publications

References 35 publications

BAX and Tumor Suppressor TRP53 Are Important in Regulating Mutagenesis in Spermatogenic Cells in Mice1

BAX and Tumor Suppressor TRP53 Are Important in Regulating Mutagenesis in Spermatogenic Cells in Mice1

Expression of full‐length and truncated Fyn tyrosine kinase transcripts and encoded proteins during spermatogenesis and localization during acrosome biogenesis and fertilization

Physiological and Pathological Cell Deaths in the Reproductive Organs.

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