Apoptosis Is Physiologically Restricted to a Specialized Cytoplasmic Compartment in Rat Spermatids

Blanco‐Rodríguez, Josefa; Martínez‐García, Carmen

doi:10.1095/biolreprod61.6.1541

Cited by 102 publications

(72 citation statements)

References 53 publications

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“…These intercytoplasmic bridges are eliminated after completion of meiosis during spermiogenesis. In mammals, caspase-1-like activity was suspected in spermatids, 40 but our results show that caspase-3 is also involved in terminal maturation of haploid cells and /or syncitia removal, and caspase-9 earlier in maturation of the spermatid heads. This agrees with the caspase-3 labeling of mature spermatozoa.…”

Section: Discussionmentioning

confidence: 50%

Caspase-independent death of meiotic and postmeiotic cells overexpressing p53: calpain involvement

et al. 2006

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In a model of male sterility (MTp53) owing to enforced p53 expression in spermatocytes II and spermatids of transgenic mice, we focused on the role of caspases. Most of them are expressed in all differentiation stages, but only the transcriptional levels of caspase-2 and caspase-3 are modified in MTp53 germ cells. In normal testis, cleaved caspase-3 and caspase-9 are detected during the elongation of spermatids. Despite this constitutive presence of caspases during terminal differentiation, calpains are the main effectors of germ cell loss in MTp53 testes: calpain 1 RNA levels are increased, caspase-3-like activity is markedly decreased while calpain activity is higher and the calpain inhibitor E64d ((2S, 3S)-trans-epoxysuccinyl-L-leucylamido-3-methylbutane ethyl ester) reduces TUNEL labeling in MTp53 testis, whereas pancaspase inhibitor zVADfmk (N-benzyloxycarbonyl-ValAla-Asp(OMe)-fluoromethylketone) has no effect. Our work suggests that despite the presence, and potent involvement, of caspases in male haploid cell maturation, calpains are the executioners of the death of terminally differentiating germ cells.

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Section: Discussionmentioning

confidence: 50%

Caspase-independent death of meiotic and postmeiotic cells overexpressing p53: calpain involvement

et al. 2006

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“…Interestingly it has been recently reported that apoptosis-like mechanisms are required for spermatid differentiation in Drosophila (Arama et al, 2003). An analogy between cytoplasmic apoptotic events and the formation of residual bodies has been also noticed in mammalian spermiogenesis (Blanco-Rodriguez and Martinez-Garcia, 1999). On the other hand, Bax was reported to be expressed, besides in spermatogonia and Sertoli cells, also in spermatocytes (Yan et al, 2000), but we found an abundant transcript in mitotic germ cells and in Sertoli cells, with the highest level of expression at 7 dpn, whereas only a very faint signal was detectable in spermatocytes (Table 1 and Fig.…”

Section: Resultsmentioning

confidence: 79%

Analysis of the gene expression profile of mouse male meiotic germ cells

Rossi

Dolci

Sette

et al. 2004

Gene Expression Patterns

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Wide genome analysis of difference in gene expression between spermatogonial populations from 7-day-old mice and pachytene spermatocytes from 18-day-old mice was performed using Affymetrix gene chips representing , 12,500 mouse known genes or EST sequences, spanning approximately 1/3rd of the mouse genome. To delineate differences in the profile of gene expression between mitotic and meiotic stages of male germ cell differentiation, expressed genes were grouped in functional clusters. The analysis confirmed the previously described pre-meiotic or meiotic expression for several genes, in particular for those involved in the regulation of the mitotic and meiotic cell cycle, and for those whose transcripts are accumulated during the meiotic stages to be translated later in post-meiotic stages. Differential expression of several additional genes was discovered. In few cases (pro-apoptotic factors Bak, Bad and Bax), data were in conflict with the previously published stage-dependent expression of genes already known to be expressed in male germ cells. Northern blot analysis of selected genes confirmed the results obtained with the microarray chips. Six of these were novel genes specifically expressed in pachytene spermatocytes: a chromatin remodeling factor (chrac1/YCL1), a homeobox gene (hmx1), a novel G-coupled receptor for an unknown ligand (Gpr19), a glycoprotein of the intestinal epithelium (mucin 3), a novel RAS activator (Ranbp9), and the A630056B21Rik gene (predicted to encode a novel zinc finger protein). These studies will help to delineate the global patterns of gene expression characterizing male germ cell differentiation for a better understanding of regulation of spermatogenesis in mammals. q

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“…Residual bodies exhibit similar protein contents and morphology, as do apoptotic bodies (Blanco-Rodriguez and Martinez-Garcia, 1999). They are pinched o by the elongated spermatids before they leave the seminiferous tubules and are then, like apoptotic bodies in the testis, phagocytized by Sertoli cells.…”

Section: Discussionmentioning

confidence: 94%

Role for c-Abl and p73 in the radiation response of male germ cells

et al. 2001

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p53 plays a central role in the induction of apoptosis of spermatogonia in response to ionizing radiation. In p53 7/ 7 testes, however, spermatogonial apoptosis still can be induced by ionizing radiation, so p53 independent apoptotic pathways must exist in spermatogonia. Here we show that the p53 homologues p63 and p73 are present in the testis and that p73, but not p63, is localized in the cytoplasm of spermatogonia. Unlike p53, neither p63 nor p73 protein levels were found to increase after a dose of 4 Gy of X-rays. Although p73 protein levels did not increase, its interaction with the nonreceptor tyrosine kinase c-Abl and its phosphorylation on tyrosine residues did. c-Abl and p73 co-localize in the cytoplasm of spermatogonia and spermatocytes and in the residual bodies. Furthermore, c-Abl protein levels increase after irradiation. p63 was not found to colocalize or interact with c-Abl neither before nor after irradiation. In conclusion, in the testis ionizing radiation elevates cytoplasmic c-Abl that in turn interacts with p73. This may represent an additional, cytoplasmic, apoptotic pathway. Although less e cient than the p53 route, this pathway may cause spermatogonial apoptosis as observed in p53 de®cient mice. Oncogene (2001) 20, 4298 ± 4304.

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Apoptosis Is Physiologically Restricted to a Specialized Cytoplasmic Compartment in Rat Spermatids

Cited by 102 publications

References 53 publications

Caspase-independent death of meiotic and postmeiotic cells overexpressing p53: calpain involvement

Caspase-independent death of meiotic and postmeiotic cells overexpressing p53: calpain involvement

Analysis of the gene expression profile of mouse male meiotic germ cells

Role for c-Abl and p73 in the radiation response of male germ cells

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