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CCR4-Associated Factor CAF1 Is an Essential Factor for Spermatogenesis

机译：CCR4相关因子CAF1是精子发生的必要因素。

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The CCR4-associated protein CAF1 has been demonstrated to play several roles in the control of transcription and of mRNA decay. To gain further insight into its physiological function, we generated CAF1-deficient mice. They are viable, healthy, and normal in appearance; however, mCAF1?/? male mice are sterile. The crossing of mCAF1+/? mice gave a Mendelian ratio of mCAF1+/+, mCAF1+/?, and mCAF1?/? pups, indicating that haploid mCAF1-deficient germ cells differentiate normally. The onset of the defect occurs during the first wave of spermatogenesis at 19 to 20 days after birth, during progression of pachytene spermatocytes to haploid spermatids and spermatozoa. Early disruption of spermatogenesis was evidenced by Sertoli cell vacuolization and tubular disorganization. The most mature germ cells were the most severely depleted, but progressively all germ cells were affected, giving Sertoli cell-only tubes, large interstitial spaces, and small testes. This phenotype could be linked to a defect(s) in germ cells and/or to inadequate Sertoli cell function, leading to seminiferous tubule disorganization and finally to a total disappearance of germ cells. The mCAF1-deficient mouse provides a new model of failed spermatogenesis in the adult that may be relevant to some cases of human male sterility.
机译：已经证明，与CCR4相关的蛋白质CAF1在转录和mRNA衰减的控制中起着多种作用。为了进一步了解其生理功能，我们生成了 CAF1 缺陷小鼠。它们是可行，健康且外观正常的;但是， mCAF1 ？/？雄性小鼠是不育的。通过对 mCAF1 + /？小鼠的杂交，孟德尔比率为 mCAF1 + / + ， mCAF1 + /？和 mCAF1 ？/？幼崽，表明单倍体 mCAF1 缺陷细胞正常分化。缺陷的发作发生在出生后19至20天的第一波精子生成过程中，在粗线期精子细胞发展为单倍体精子和精子的过程中。 Sertoli细胞空泡化和肾小管组织紊乱证明了精子发生的早期破坏。最成熟的生殖细胞耗竭最严重，但逐渐影响了所有生殖细胞，形成了仅支持细胞的试管，较大的间隙和较小的睾丸。这种表型可能与生殖细胞的缺陷和/或Sertoli细胞功能不足有关，从而导致生精小管紊乱并最终导致生殖细胞完全消失。 mCAF1 缺陷小鼠提供了成年后精子发生失败的新模型，这可能与某些男性不育病例有关。

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