MORE MOG GENES THAT INFLUENCE THE SWITCH FROM SPERMATOGENESIS TO OOGENESIS IN THE HERMAPHRODITE GERM-LINE OF CAENORHABDITIS-ELEGANS

被引:75
|
作者
GRAHAM, PL
SCHEDL, T
KIMBLE, J
机构
[1] UNIV WISCONSIN,MOLEC BIOL LAB,MADISON,WI 53706
[2] NORTHWESTERN UNIV,SCH MED,DEPT CMS BIOL,CHICAGO,IL 60611
[3] WASHINGTON UNIV,SCH MED,DEPT GENET,ST LOUIS,MO 63110
来源
DEVELOPMENTAL GENETICS | 1993年 / 14卷 / 06期
关键词
SEX DETERMINATION; TRANSLATIONAL CONTROL; GERM LINE; C-ELEGANS; MOG GENES;
D O I
10.1002/dvg.1020140608
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The Caenorhabditis elegans XX animal possesses a hermaphrodite germ line, producing first sperm, then oocytes. In this paper, we report the genetic identification of five genes, mog-2, mog-3, mog-4, mog-5, and mog-6, that influence the hermaphrodite switch from spermatogenesis to oogenesis. In mog-2-mog-6 mutants, spermatogenesis continues past the time at which hermaphrodites normally switch into oogenesis and no oocytes are observed. Therefore, in these mutants, germ cells are transformed from a female fate (oocyte) to a male fate (sperm). The fem-3 gene is one of five genes that acts at the end of the germline sex determination pathway to direct spermatogenesis. Analyses of mog;fem-3 double mutants suggest that the mog-2-mog-6 genes act before fem-3; thus these genes may be in a position to negatively regulate fem-3 or one of the other terminal regulators of germline sex determination. Double mutants of fem-3 and any one of the meg mutations make oocytes. Using these double mutants, we show that oocytes from any mog;fem-3 double mutant are defective in their ability to support embryogenesis. This maternal effect lethality indicates that each of the meg genes is required for embryogenesis. The two defects in mog-2-mog-6 mutants are similar to those of mog-1: all six meg genes eliminate the sperm/oocyte switch in hermaphrodites and cause maternal effect lethality. We propose that the mog-2-mog-6 mutations identify genes that act with mog-1 to effect the sperm/oocyte switch. We further speculate that the mog-1-mog-6 mutations all interfere with translational controls of fem-3 and other maternal mRNAs. (C) 1993 Wiley-Liss, Inc.
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页码:471 / 484
页数:14
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