Molecular Mechanisms for the Regulation of Meiosis

1.筛选了减数分裂缺陷突变体meiRNA的抑制子，并分离了减数分裂特异性基因mei 4、spo 5、ssm 4等。事实证明，这种抑制不是由它们的蛋白质产物引起的，而是由它们的部分mRNA引起的。有趣的是，这些mRNA是不稳定的，即使人工表达，也不会在有丝分裂生长的细胞中积累，并且导致这种不稳定性的区域与抑制meiRNA损失的区域重叠。因此，我们推测这些mRNA携带一个区域，使它们在有丝分裂细胞周期中不稳定，并且在减数分裂期间有某种机制起稳定作用。2.分裂酵母Mei 2 p，减数分裂起始的调节剂，在前期I核中形成点结构。我们已经证明，这个点是Mei 2 p和新生meiRNA的复合物，只是从基因转录而来。3.我们分离到一个新的裂殖酵母tor 1突变体，它编码一种性发育所需的TOR激酶。然后，我们分离gad 8，它编码的AGC家族的激酶，作为该突变体的抑制剂。分析表明，Tor 1 p通过Gad 8 p调节性发育和应激反应。4.分离出C. elegans DAZ-1，DAZ的同源物，负责哺乳动物的无精子症。在DAZ-1缺陷的蠕虫，减数分裂过程中被逮捕在粗线期卵子发生。它们在生殖腺的增殖期甚至在生殖细胞中都表现出异常的核形态。DAZ-1缺陷型蠕虫在减数分裂阶段的生殖细胞中既没有显示核仁的扩张，也没有形成中央细胞质核心，并且这些细胞在蛋白质合成中似乎不太活跃。其他数据表明DAZ-1也可能参与性腺的性转换。

1.We screened for suppressors of the fission yeast meiosis-defective mutant lacking meiRNA, which is indispensable for meiosis I, and isolated meiosis-specific genes mei4, spo5, ssm4 and others. It turned out that the suppression was caused not by their protein products but by part of their mRNAs. Interestingly, these mRNAs were unstable and did not accumulate in mitotically growing cells, even if artificially expressed, and the region responsible for this instability overlapped with the region that suppressed loss of meiRNA. Thus we speculate that these mRNAs carry a region that renders them unstable in the mitotic cell cycle, and that a certain mechanism operates to stabilize them during meiosis. 2.Fission yeast Mei2p, the regulator of the initiation of meiosis, forms a dot structure in prophase I nuclei. We have demonstrated that this dot is a complex of Mei2p and nascent meiRNA, just transcribed from the gene. 3.We isolate a new mutant of fission yeast tor1, which encodes a TOR kinase required for sexual development. We then isolated gad8, which encoded a kinase of the AGC family, as a suppressor of this mutant. Analysis has shown that Tor1p regulates sexual development and stress responses through Gad8p. 4.We isolated C. elegans DAZ-1, a homolog of DAZ responsible for azoospermia in mammals. In DAZ-1-defective worms, the meiotic process was arrested at pachytene during oogenesis. They showed abnormal nuclear morphology even in germ cells at the proliferative stage in the gonad. The DAZ-1-defective worms did not show expansion of nucleoli nor formation of the central cytoplasmic core in germ cells at the meiotic stage, and these cells appeared to be less active in protein synthesis. Other data have suggested that DAZ-1 may also be involved in switching sexuality of the gonad.