gon-4, a cell lineage regulator required for gonadogenesis in Caenorhabditis elegans

被引:34
作者
Friedman, L
Santa Anna-Arriola, S
Hodgkin, J
Kimble, J
机构
[1] Univ Wisconsin, Dept Biochem, Howard Hughes Med Inst, Madison, WI 53706 USA
[2] Univ Wisconsin, Mol Biol Lab, Madison, WI 53706 USA
[3] Univ Wisconsin, Dept Med Genet, Madison, WI 53706 USA
[4] MRC, Mol Biol Lab, Cambridge CB2 2QH, England
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
cell lineage; organogenesis; Caenorhabditis elegans; gonad; gon-4; cell cycle;
D O I
10.1006/dbio.2000.9944
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The gon-4 gene is required for gonadogenesis in the nematode Caenorhabditis elegans. Normally, two precursor cells, Z1 and Z4, follow a reproducible pattern of cell divisions to generate the mature somatic gonadal structures (e.g., uterus in hermaphrodites, vas deferens in males). In contrast, in gon-4 mutants, the Z1/Z4 cell lineages are variably aborted in both hermaphrodites and males: Z1 and Z4 divide much later than normal and subsequent divisions are either absent or severely delayed. In gon-4 adults, normal somatic gonadal structures are never observed, and germ-line and vulval tissues, which depend on somatic gonadal cues for their development, are also aberrant. In contrast, nongonadal tissues and the timing of other developmental events (e.g., molts) appear to be normal in gon-4 mutants. The gon-4 alleles are predicted to be strong loss-of-function or null alleles by both genetic and molecular criteria. We have cloned gon-4 in an attempt to learn how it regulates gonadogenesis. The gon-4 gene encodes a novel, acidic protein. A GON-4::GFP fusion protein, which rescues a gon-4 mutant to fertility, is expressed in somatic gonadal cells during early gonadal development. Furthermore, this fusion protein is nuclear. We conclude that gon-4 is a regulator of the early lineage of Z1 and Z4 and suggest that it is a part of a genetic program common to the regulation of both hermaphrodite and male gonadogenesis. (C) 2000 Academic Press.
引用
收藏
页码:350 / 362
页数:13
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