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秀丽隐杆线虫减数分裂起始的遗传调控。

Genetic regulation of entry into meiosis in Caenorhabditis elegans.

作者信息

Kadyk L C, Kimble J

机构信息

Howard Hughes Medical Institute, Department of Biochemistry, University of Wisconsin, Madison, Wisconsin 53706, USA.

出版信息

Development. 1998 May;125(10):1803-13. doi: 10.1242/dev.125.10.1803.

Abstract

The Caenorhabditis elegans germline is composed of mitotically dividing cells at the distal end that give rise to meiotic cells more proximally. Specification of the distal region as mitotic relies on induction by the somatic distal tip cell and the glp-1 signal transduction pathway. However, the genetic control over the transition from mitosis to meiosis is not understood. In this paper, we report the identification of a gene, gld-2, that has at least two functions in germline development. First, gld-2 is required for normal progression through meiotic prophase. Second, gld-2 promotes entry into meiosis from the mitotic cell cycle. With respect to this second function, gld-2 appears to be functionally redundant with a previously described gene, gld-1 (Francis, R., Barton, M. K., Kimble, J. and Schedl, T. (1995) Genetics 139, 579-606). Germ cells in gld-1(o) and gld-2 single mutants enter meiosis at the normal time, but germ cells in gld-2 gld-1(o) double mutants do not enter meiosis. Instead, the double mutant germline is mitotic throughout and forms a large tumor. We suggest that gld-1 and gld-2 define two independent regulatory pathways, each of which can be sufficient for entry into meiosis. Epistasis analyses show that gld-1 and gld-2 work downstream of the glp-1 signal transduction pathway. Therefore, we hypothesize that glp-1 promotes proliferation by inhibiting the meiosis-promoting functions of gld-1 and gld-2.

摘要

秀丽隐杆线虫的生殖系由远端进行有丝分裂的细胞组成,这些细胞向近端产生减数分裂细胞。远端区域作为有丝分裂区域的特化依赖于体细胞远端末梢细胞的诱导和glp-1信号转导途径。然而,从有丝分裂向减数分裂转变的遗传控制尚不清楚。在本文中,我们报告了一个基因gld-2的鉴定,该基因在生殖系发育中至少具有两种功能。首先,gld-2是减数分裂前期正常进程所必需的。其次,gld-2促进从有丝分裂细胞周期进入减数分裂。关于这第二种功能,gld-2似乎与先前描述的基因gld-1在功能上冗余(弗朗西斯,R.,巴顿,M.K.,金布尔,J.和施德尔,T.(1995年)《遗传学》139卷,579 - 606页)。gld-1(o)和gld-2单突变体中的生殖细胞在正常时间进入减数分裂,但gld-2 gld-1(o)双突变体中的生殖细胞不进入减数分裂。相反,双突变体的生殖系始终进行有丝分裂并形成一个大肿瘤。我们认为gld-1和gld-2定义了两条独立的调控途径,每条途径都足以促使细胞进入减数分裂。上位性分析表明,gld-1和gld-2在glp-1信号转导途径的下游起作用。因此,我们假设glp-1通过抑制gld-1和gld-2促进减数分裂的功能来促进增殖。

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