Kashiwabara Shin-Ichi, Noguchi Junko, Zhuang Tiangang, Ohmura Ko, Honda Arata, Sugiura Shin, Miyamoto Kiyoko, Takahashi Satoru, Inoue Kimiko, Ogura Atsuo, Baba Tadashi
Institute of Applied Biochemistry, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba Science City, Ibaraki 305-8572, Japan.
Science. 2002 Dec 6;298(5600):1999-2002. doi: 10.1126/science.1074632.
Spermatogenesis is a highly specialized process of cellular differentiation to produce spermatozoa. This differentiation process accompanies morphological changes that are controlled by a number of genes expressed in a stage-specific manner during spermatogenesis. Here we show that in mice, the absence of a testis-specific, cytoplasmic polyadenylate [poly(A)] polymerase, TPAP, results in the arrest of spermiogenesis. TPAP-deficient mice display impaired expression of haploid-specific genes that are required for the morphogenesis of germ cells. The TPAP deficiency also causes incomplete elongation of poly(A) tails of particular transcription factor messenger RNAs. Although the overall cellular level of the transcription factor TAF10 is unaffected, TAF10 is insufficiently transported into the nucleus of germ cells. We propose that TPAP governs germ cell morphogenesis by modulating specific transcription factors at posttranscriptional and posttranslational levels.
精子发生是一个高度特化的细胞分化过程,用以产生精子。这一分化过程伴随着形态学变化,这些变化由许多在精子发生过程中以阶段特异性方式表达的基因所控制。在此我们表明,在小鼠中,睾丸特异性的细胞质聚腺苷酸[聚(A)]聚合酶TPAP的缺失会导致精子形成停滞。TPAP缺陷型小鼠表现出单倍体特异性基因表达受损,而这些基因是生殖细胞形态发生所必需的。TPAP缺陷还会导致特定转录因子信使核糖核酸的聚(A)尾巴不完全延长。尽管转录因子TAF10的整体细胞水平未受影响,但TAF10无法充分转运到生殖细胞的细胞核中。我们提出,TPAP通过在转录后和翻译后水平调节特定转录因子来控制生殖细胞的形态发生。