Littlefield C L, Finkemeier C, Bode H R
Developmental Biology Center, University of California, Irvine 92717.
Dev Biol. 1991 Aug;146(2):292-300. doi: 10.1016/0012-1606(91)90231-q.
Hydra oligactis undergo two mutually exclusive modes of reproduction: at warm temperatures (18-22 degrees C) animals reproduce asexually by budding, while at cold temperatures (10-12 degrees C) gamete differentiation occurs. Using a monoclonal antibody which is specific for cells of the sperm lineage, it was discovered that under conditions where sperm differentiation does not occur (18-22 degrees C), cells continually enter the sperm pathway but progression down the pathway is prematurely halted, effectively blocking the production of sperm. To elucidate the mechanism by which completion of sperm differentiation is controlled, the cell cycle times of interstitial cells entering the sperm pathway at both the restrictive (18 degrees C) and permissive (10 degrees C) temperatures were examined. It was envisaged that at the restrictive temperature the cell cycle times of committed cells would lengthen as they proceeded down the pathway, leading to dilution and eventual loss of cells at later stages of sperm differentiation. This did not occur. Although cells of the sperm lineage were found overall to divide more slowly at 18 degrees C than at 10 degrees C, at both temperatures the cell cycle times shortened as cells proceeded further down the pathway, making a dilution mechanism untenable. The effect of high temperature on the survival of cells was then tested by subjecting animals to a heat shock. Within 12 hr of the increase in temperature, the total number of sperm lineage interstitial cells dropped 10-fold while the total numbers of epithelial and somatic interstitial cells remained virtually unchanged. A distinct consequence of this cell loss was the disappearance of cells furthest down the sperm pathway. It is proposed that as cells move down the sperm pathway, they become increasingly sensitive to high temperature which adversely affects their survival; the higher the temperature, the earlier in the pathway cells die. The lethal effect is abolished by lowering the temperature, allowing sperm differentiation to continue to completion. The possible adaptive advantages of temperature controlling gametogenesis are discussed.
在温暖温度（18 - 22摄氏度）下，动物通过出芽进行无性繁殖，而在寒冷温度（10 - 12摄氏度）下，会发生配子分化。使用一种对精子谱系细胞特异的单克隆抗体，发现了在精子分化不发生的条件下（18 - 22摄氏度），细胞持续进入精子生成途径，但在该途径中的进程过早停止，有效地阻止了精子的产生。为了阐明控制精子分化完成的机制，研究了在限制温度（18摄氏度）和允许温度（10摄氏度）下进入精子生成途径的间质细胞的细胞周期时间。据设想，在限制温度下，已定向的细胞在沿着途径前进时细胞周期时间会延长，导致在精子分化后期细胞稀释并最终丢失。但实际并非如此。尽管总体上发现精子谱系的细胞在18摄氏度时比在10摄氏度时分裂更慢，但在两个温度下，随着细胞在途径中进一步前进，细胞周期时间都缩短了，这使得稀释机制难以成立。然后通过对动物进行热休克来测试高温对细胞存活的影响。在温度升高后的12小时内，精子谱系间质细胞的总数下降了10倍，而上皮和体间质细胞的总数几乎保持不变。这种细胞损失的一个明显后果是精子生成途径最下游的细胞消失了。有人提出，随着细胞沿着精子生成途径移动，它们对高温变得越来越敏感。高温会对它们的存活产生不利影响；温度越高，细胞在途径中死亡得越早。降低温度可消除这种致死效应，使精子分化能够继续完成。文中还讨论了温度控制配子发生可能具有的适应性优势。
