By Jonathan L. Tilly, Jerome F. Strauss, Martin Tenniswood
The law of cellphone dying in quite a few reproductive tissues, as in different ma jor organ structures of the physique, has develop into a focus of study task in lots of laboratories during the last few years. As such, the necessity for a "for mal" assembly to spotlight contemporary paintings during this box, in addition to to combine wisdom from different assets (such as investigators engaged on cellphone dying in melanoma and immune functionality) within the vast context of picking con served pathways that coordinate life-and-death judgements in varied phone kinds, turned obvious. hence, the ambitions of the medical Committee of the overseas Symposium on mobilephone dying in Reproductive body structure, spon sored by way of Serono Symposia united states, have been already predetermined via this desire. easily acknowledged, we sought to collect for the 1st time a pick out cohort of reproductive biologists and telephone dying researchers, many yet now not all cho sen in accordance with their pioneering efforts in elucidating the basic features of apoptosis in reproductive and nonreproductive tissues, as a way to re view the present prestige of the sphere, foster new rules, and advertise clinical collaborations. within the resulting chapters of this e-book, summaries of labor dis stubborn on the assembly are awarded to stress either the range and the similarities within the prevalence and law of apoptosis in tissues of the female and male reproductive systems.
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Additional resources for Cell Death in Reproductive Physiology
Cells were not immunostained at the beginning of culture (A) but became strongly positive after 16-18 h of culure (B). ) against mouse BCL-2 p25 protein was employed. Magnification, 500X. decreases the number of oocytes and primordial follicles endowed in mouse ovaries. Using RT-PCR (data not shown), immunohistochemistry, and Western blotting (Figs. 9), we did not obtain evidence that addition of MR(K) TO c lL. 9. Western blot analysis of BCL-2 expression in germ cells freshly collected (To) or cultured for 16-18 h without (C) or with 100 ng/ml SCF.
And the meeting's scientific committee-Jon Tilly, Jerome Strauss III, and Martin Tenniswood-for bringing this meeting and publication to fruition. Some nematode strains used in this research were provided by the Caenorhabditis Genetics Center, which is funded by the NIH National Center for Research Resources (NCRR). MOH is a Rita Allen Foundation scholar. Work in the authors' laboratory is supported by PHS grant ROI-GM52540. References I. Thompson CB. Apoptosis in the pathogenesis and treatment of disease.
Mutations in ced-9 that reduce or eliminate its function allow excessive cell death to occur (22). Null mutations confer maternal-effect lethality, where homozygous mutant offspring of a heterozygous parent survive, but selfprogeny of a homozygous mutant parent die as embryos. Interestingly, homozygous mutants of a heterozygous mother may survive, but they lay fewer embryos, suggesting that ced-9 function affects not only viability, but also fertility. Indeed, germ cell death is increased in ced-9(lj) animals, suggesting that ced-9 has a protective function in the germline, as it does in the soma (unpublished observations).