The mog-1 gene is required for the switch from spermatogenesis to oogenesis in Caenorhabditis elegans.
The mog-1 gene is required for the switch from spermatogenesis to oogenesis in Caenorhabditis elegans.
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mog-1 基因是秀丽隐杆线虫从精子发生到卵子发生的转变所必需的。
DOI：
10.1093/genetics/133.4.919
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发表时间：
1993
期刊：
影响因子：
3.3
通讯作者：
Kimble,J
中科院分区：
文献类型：
--
作者：
Graham,PL;Kimble,J
秀丽隐杆线虫雌雄同体首先产生精子，然后产生卵母细胞。相比之下，基因 mog-1（用于生殖系男性化）中六种功能丧失突变中任何一种的纯合动物会持续产生精子，并且不会转变为卵子发生。因此，在mog-1突变体中，通常会成为卵母细胞的生殖细胞被转化为精子。相比之下，体细胞性命运是正常的，这表明 mog-1 在性别决定中发挥着种系特异性的作用。双突变体的分析表明，mog-1 负向调节 fem 基因和/或fog-1：mog-1； fem 和 mog-1； fog-1双突变体都产生卵母细胞而不是精子。因此，我们认为野生型 mog-1 在雌雄同体种系中是必需的，用于调节从精子发生到卵子发生的转换，而不是用于规范卵子发生本身。除了在种系性别决定中的作用外，母体 mog-1 也是胚胎发生所必需的：大多数 mog-1 的后代； fem 或 mog-1； folg-1 母亲在胚胎时死亡。 mog-1 在精子/卵母细胞转换和胚胎发生中的作用如何联系起来？先前的研究表明，fem-3 通过转录后调节来实现精子/卵母细胞的转换。我们推测 mog-1 可能在多种种系 RNA（包括 fem-3）的转录后调控中发挥作用。 mog-1的缺失可能会不适当地激活fem-3，从而废除精子/卵母细胞的转换；它的缺失还可能导致母体 RNA 的失调，从而导致胚胎死亡。
Caenorhabditis elegans hermaphrodites make first sperm, then oocytes. By contrast, animals homozygous for any of six loss-of-function mutations in the gene mog-1 (for masculinization of the germ line) make sperm continuously and do not switch into oogenesis. Therefore, in mog-1 mutants, germ cells that normally would become oocytes are transformed into sperm. By contrast, somatic sexual fates are normal, suggesting that mog-1 plays a germ line-specific role in sex determination. Analyses of double mutants suggest that mog-1 negatively regulates the fem genes and/or fog-1: mog-1; fem and mog-1; fog-1 double mutants all make oocytes rather than sperm. Therefore, we propose that wild-type mog-1 is required in the hermaphrodite germ line for regulation of the switch from spermatogenesis to oogenesis rather than for specification of oogenesis per se. In addition to its role in germline sex determination, maternal mog-1 is required for embryogenesis: most progeny of a mog-1; fem or mog-1; fog-1 mother die as embryos. How might the roles of mog-1 in the sperm/oocyte switch and embryogenesis be linked? Previous work showed that fem-3 is regulated post-transcriptionally to achieve the sperm/oocyte switch. We speculate that mog-1 may function in the post-transcriptional regulation of numerous germ-line RNAs, including fem-3. A loss of mog-1 might inappropriately activate fem-3 and thereby abolish the sperm/oocyte switch; its loss might also lead to misregulation of maternal RNAs and thus embryonic death.