Institute of Molecular and Cellular Biology, National Taiwan University, Taipei, Taiwan 10617, Republic of China.
Mol Biol Cell. 2011 Jun 1;22(11):1878-86. doi: 10.1091/mbc.E10-12-1011. Epub 2011 Apr 6.
In budding yeast, the Ndt80 protein is a meiosis-specific transcription factor that is essential for the exit of pachytene and progression into nuclear divisions and spore formation. The pachytene checkpoint responds to defects in meiotic recombination and chromosome synapsis and negatively regulates the activity of Ndt80. The activity of Ndt80 was suggested to be regulated at both transcriptional and posttranslational levels; however, the mechanism for posttranslational regulation of Ndt80 was unclear. From a study of ndt80 in-frame deletion mutations, we have identified a dominant mutation NDT80-bc, which is able to completely bypass the pachytene checkpoint. The NDT80-bc mutation relieves the checkpoint-mediated arrest of the zip1, dmc1, and hop2 mutants, producing spores with low viability. The NDT80-bc mutant provides direct evidence for the posttranslational control of Ndt80 activity. Furthermore, the data presented show that Ndt80 is retained in cytoplasm in the zip1 mutant, whereas Ndt80-bc is found in the nucleus. We propose that the nuclear localization of Ndt80 is regulated by the pachytene checkpoint through a cytoplasmic anchor mechanism.
在芽殖酵母中，Ndt80 蛋白是一种减数分裂特异性转录因子，对于从粗线期退出并进入核分裂和孢子形成是必不可少的。粗线期检查点响应减数分裂重组和染色体联会的缺陷，并负调控 Ndt80 的活性。Ndt80 的活性被认为受到转录和翻译后水平的调节；然而，Ndt80 的翻译后调节机制尚不清楚。通过对 ndt80 框内缺失突变的研究，我们鉴定了一个显性突变 NDT80-bc，它能够完全绕过粗线期检查点。NDT80-bc 突变缓解了 zip1、dmc1 和 hop2 突变体中检查点介导的阻滞，产生了低活力的孢子。NDT80-bc 突变体为 Ndt80 活性的翻译后控制提供了直接证据。此外，所呈现的数据表明，在 zip1 突变体中 Ndt80 保留在细胞质中，而 Ndt80-bc 存在于细胞核中。我们提出，通过细胞质锚定机制，Ndt80 的核定位受到粗线期检查点的调节。
