Tenenhaus C, Subramaniam K, Dunn M A, Seydoux G
Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Genes Dev. 2001 Apr 15;15(8):1031-40. doi: 10.1101/gad.876201.
The CCCH zinc finger protein PIE-1 is an essential regulator of germ cell fate that segregates with the germ lineage during the first cleavages of the Caenorhabditis elegans embryo. We have shown previously that one function of PIE-1 is to inhibit mRNA transcription. Here we show that PIE-1 has a second function in germ cells; it is required for efficient expression of the maternally encoded Nanos homolog NOS-2. This second function is genetically separable from PIE-1's inhibitory effect on transcription. A mutation in PIE-1's second CCCH finger reduces NOS-2 expression without affecting transcriptional repression and causes primordial germ cells to stray away from the somatic gonad, occasionally exiting the embryo entirely. Our results indicate that PIE-1 promotes germ cell fate by two independent mechanisms as follows: (1) inhibition of transcription, which blocks zygotic programs that drive somatic development, and (2) activation of protein expression from nos-2 and possibly other maternal RNAs, which promotes primordial germ cell development.
CCCH锌指蛋白PIE-1是生殖细胞命运的关键调节因子,在秀丽隐杆线虫胚胎的首次分裂过程中与生殖谱系分离。我们之前已经表明PIE-1的一个功能是抑制mRNA转录。在此我们表明PIE-1在生殖细胞中还有第二个功能;它是母源编码的Nanos同源物NOS-2高效表达所必需的。这第二个功能在遗传上可与PIE-1对转录的抑制作用相分离。PIE-1第二个CCCH指中的一个突变会降低NOS-2的表达,而不影响转录抑制,并导致原始生殖细胞偏离体细胞性腺,偶尔会完全离开胚胎。我们的结果表明,PIE-1通过以下两种独立机制促进生殖细胞命运:(1)抑制转录,这会阻断驱动体细胞发育的合子程序;(2)激活nos-2以及可能其他母源RNA的蛋白表达,这会促进原始生殖细胞发育。