Heat shock transcription factor 1 is involved in quality-control mechanisms in male germ cells
Heat shock transcription factor 1 is involved in quality-control mechanisms in male germ cells
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DOI：
10.1095/biolreprod.103.020065
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发表时间：
2004-01-01
影响因子：
3.6
通讯作者：
Nakai, A
中科院分区：
文献类型：
--
作者：
Izu, H;Inouye, S;Nakai, A
精子发生中的质量控制机制对于消除受损或异常细胞非常重要，从而保护生物体在下一代中免受异常发育。精子发生的过程对高温高度敏感;然而，受损生殖细胞被清除的机制仍不清楚。在这里，我们发现，热休克蛋白不诱导雄性生殖细胞在热应激反应，虽然热休克转录因子1（HSF 1）被激活。使用HSF 1基因敲除小鼠，我们发现，粗线期精母细胞的凋亡显着抑制在睾丸与一个单一的暴露于热和隐睾，表明HSF 1促进粗线期精母细胞的凋亡细胞死亡暴露于热应激。与此形成鲜明对比的是，在暴露于高温的睾丸中，HSF 1作为更多未成熟生殖细胞（可能包括精原细胞）的细胞存活因子。这些结果表明，热休克因子1在男性生殖细胞中具有两种相反的作用，独立于热休克基因的激活。
Quality-control mechanisms in spermatogenesis are important to eliminate injured or abnormal cells, thereby protecting the organism from abnormal development in the next generation. The processes of spermatogenesis are highly sensitive to high temperatures; however, the mechanisms by which injured germ cells are eliminated remain unclear. Here, we found that heat shock proteins are not induced in male germ cells in response to thermal stress, although heat shock transcription factor 1 (HSF1) is activated. Using HSF1-null mice, we showed that apoptosis of pachytene spermatocytes was markedly inhibited in testes with a single exposure to heat and in the cryptorchid testes, indicating that HSF1 promotes apoptotic cell death of pachytene spermatocytes exposed to thermal stress. In marked contrast, HSF1 acts as a cell-survival factor of more immature germ cells, probably including spermatogonia, in testes exposed to high temperatures. These results demonstrate that HSF1 has two opposite roles in male germ cells independent of the activation of heat shock genes.