Arrest of spermatogenesis in mice expressing an active heat shock transcription factor 1
Arrest of spermatogenesis in mice expressing an active heat shock transcription factor 1
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DOI：
10.1093/emboj/19.7.1545
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发表时间：
2000-04-03
期刊：
影响因子：
11.4
通讯作者：
Tanabe, M
中科院分区：
文献类型：
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作者：
Nakai, A;Suzuki, M;Tanabe, M
在哺乳动物中，睾丸温度低于核心体温，精子发生对热伤害的脆弱本质已经被知道了一个世纪。然而，受气温上升影响的主要目标尚不明确。我们在这里报道，在睾丸中表达活性形式的热休克转录因子1(HSF1)的雄性小鼠由于精子发生障碍而不育。生殖细胞进入减数分裂前期，滞留在粗线期，凋亡生殖细胞数量显著增加。在野生型小鼠中，单次热暴露可引起HSF1的激活，以及类似的组织学变化，如粗线期精母细胞的特异性凋亡。这些结果表明，热损伤导致的男性不育至少部分是由于HSF1的激活，导致初级精母细胞发生凋亡。
In mammals, testicular temperature is lower than core body temperature, and the vulnerable nature of spermatogenesis to thermal insult has been known for a century. However, the primary target affected by increases in temperature is not yet clear. We report here that male mice expressing an active form of heat shock transcription factor 1 (HSF1) in the testis are infertile due to a block in spermatogenesis. The germ cells entered meiotic prophase and were arrested at pachytene stage, and there was a significant increase in the number of apoptotic germ cells in these mice. In wild-type mice, a single heat exposure caused the activation of HSF1 and similar histological changes such as a stage-specific apoptosis of pachytene spermatocytes, These results suggest that male infertility caused by thermal insult is at least partly due to the activation of HSF1, which induces the primary spermatocytes to undergo apoptosis.