Tenenhaus C, Schubert C, Seydoux G
School of Medicine, Johns Hopkins University, Baltimore, Maryland, 21205-2185, USA.
Dev Biol. 1998 Aug 15;200(2):212-24. doi: 10.1006/dbio.1998.8940.
In early Caenorhabditis elegans embryos, production of new mRNAs is inhibited in the germ lineage. This inhibition requires the germline factor PIE-1, and correlates with the absence in germline blastomeres of a phosphoepitope on RNA polymerase II (RNAPII-H5). We show that PIE-1 is uniformly distributed in oocytes and newly fertilized eggs, and becomes localized asymmetrically in the late one-cell stage. To begin to dissect the mechanisms required for PIE-1 localization and inhibition of RNAPII-H5 expression, we have examined the distribution of PIE-1 and RNAPII-H5 in maternal-effect mutants that disrupt embryonic development. We find that mutants that disrupt the asymmetric divisions of germline blastomeres mislocalize PIE-1, and activate RNAPII-H5 expression in the germ lineage. In contrast, mutants that alter somatic cell identities do not affect PIE-1 localization or RNAPII-H5 expression. Our observations suggest that PIE-1 represses mRNA transcription in each germline blastomere in a concentration-dependent manner. We also show that in wild-type, and in mutants where PIE-1 is mislocalized, the cellular and subcellular distribution of PIE-1 remarkably parallels that of the P granules, suggesting that the localizations of these two germline components are coordinately regulated.
在早期秀丽隐杆线虫胚胎中，生殖谱系中新生mRNA的产生受到抑制。这种抑制作用需要生殖系因子PIE-1，并且与生殖系卵裂球中RNA聚合酶II上的一个磷酸化表位（RNAPII-H5）的缺失相关。我们发现，PIE-1在卵母细胞和新受精的卵子中均匀分布，并在单细胞晚期不对称定位。为了开始剖析PIE-1定位和抑制RNAPII-H5表达所需的机制，我们研究了破坏胚胎发育的母系效应突变体中PIE-1和RNAPII-H5的分布。我们发现，破坏生殖系卵裂球不对称分裂的突变体使PIE-1定位错误，并在生殖谱系中激活RNAPII-H5的表达。相比之下，改变体细胞身份的突变体不影响PIE-1的定位或RNAPII-H5的表达。我们的观察结果表明，PIE-1以浓度依赖的方式抑制每个生殖系卵裂球中的mRNA转录。我们还表明，在野生型以及PIE-1定位错误的突变体中，PIE-1的细胞和亚细胞分布与P颗粒的分布非常相似，这表明这两种生殖系成分的定位受到协同调节。
