Kashiwabara Shin-Ichi, Tsuruta Satsuki, Okada Keitaro, Yamaoka Yutaro, Baba Tadashi
Faculty of Life and Environmental Sciences, University of Tsukuba, Ibaraki 305-8572, Japan.
J Reprod Dev. 2016 Dec 20;62(6):607-614. doi: 10.1262/jrd.2016-116. Epub 2016 Sep 18.
The testis-specific cytoplasmic poly(A) polymerase PAPOLB/TPAP is essential for spermatogenesis. Although this enzyme is responsible for poly(A) tail extension of a subset of mRNAs in round spermatids, the stability and translational efficiency of these mRNAs are unaffected by the absence of PAPOLB. To clarify the functional importance of this enzyme's adenylation activity, we produced PAPOLB-null mice expressing a polyadenylation-defective PAPOLB mutant (PAPOLB), in which the catalytic Asp at residue 114 was mutated to Ala. Introducing PAPOLB failed to rescue PAPOLB-null phenotypes, such as reduced expression of haploid-specific mRNAs, spermiogenesis arrest, and male infertility. These results suggest that PAPOLB regulates spermatogenesis through its adenylation activity.
睾丸特异性胞质多聚腺苷酸聚合酶PAPOLB/TPAP对精子发生至关重要。尽管这种酶负责圆形精子细胞中一部分mRNA的多聚腺苷酸尾延伸,但这些mRNA的稳定性和翻译效率不受PAPOLB缺失的影响。为了阐明这种酶的腺苷化活性的功能重要性,我们制备了表达多聚腺苷酸化缺陷型PAPOLB突变体(PAPOLB)的PAPOLB基因敲除小鼠,其中第114位残基的催化天冬氨酸被突变为丙氨酸。引入PAPOLB未能挽救PAPOLB基因敲除的表型,如单倍体特异性mRNA表达降低、精子发生停滞和雄性不育。这些结果表明,PAPOLB通过其腺苷化活性调节精子发生。