Strome S, Martin P, Schierenberg E, Paulsen J
Department of Biology, Indiana University, Bloomington 47405, USA.
Development. 1995 Sep;121(9):2961-72. doi: 10.1242/dev.121.9.2961.
Mutations in the maternal-effect sterile gene mes-1 cause the offspring of homozygous mutant mothers to develop into sterile adults. Lineage analysis revealed that mutant offspring are sterile because they fail to form primordial germ cells during embryogenesis. In wild-type embryos, the primordial germ cell P4 is generated via a series of four unequal stem-cell divisions of the zygote. mes-1 embryos display a premature and progressive loss of polarity in these divisions: P0 and P1 undergo apparently normal unequal divisions and cytoplasmic partitioning, but P2 (in some embryos) and P3 (in most embryos) display defects in cleavage asymmetry and fail to partition lineage-specific components to only one daughter cell. As an apparent consequence of these defects, P4 is transformed into a muscle precursor, like its somatic sister cell D, and generates up to 20 body muscle cells instead of germ cells. Our results show that the wild-type mes-1 gene participates in promoting unequal germ-line divisions and asymmetric partitioning events and thus the determination of cell fate in early C. elegans embryos.
母源性不育基因mes-1的突变会导致纯合突变体母亲的后代发育为不育成虫。谱系分析表明,突变体后代不育是因为它们在胚胎发育过程中未能形成原始生殖细胞。在野生型胚胎中,原始生殖细胞P4是通过合子的一系列四次不等干细胞分裂产生的。mes-1胚胎在这些分裂中表现出极性的过早和渐进丧失:P0和P1经历明显正常的不等分裂和细胞质分配,但P2(在一些胚胎中)和P3(在大多数胚胎中)在卵裂不对称方面存在缺陷,并且未能将谱系特异性成分仅分配给一个子细胞。作为这些缺陷的明显后果,P4像其体细胞姐妹细胞D一样转变为肌肉前体细胞,并产生多达20个身体肌肉细胞而非生殖细胞。我们的结果表明,野生型mes-1基因参与促进不等的种系分裂和不对称分配事件,从而参与秀丽隐杆线虫早期胚胎细胞命运的决定。