Shanks Robert M Q, Bascom-Slack Carol, Dawson Dean S
Department of Microbiology and Immunology, Dartmouth Medical School, Hanover, New Hampshire, USA.
Cell Cycle. 2004 Mar;3(3):363-71. Epub 2004 Mar 1.
The motor protein Kar3p and its associated protein Cik1p are essential for passage through meiosis I. In the absence of either protein, meiotic cells arrest in prophase I. Experiments were performed to determine whether the arrest was caused by a structural inability to proceed through meiosis, or by a regulatory mechanism. The data demonstrate that the meiotic arrest is not structural; kar3 and cik1 mutants are able to form normal looking bipolar spindles and divide their DNA into two masses in spo11 mutant backgrounds. To identify the regulatory system necessary for the kar3/cik1 meiotic arrest, we tested whether the arrest could be bypassed by eliminating the pachytene checkpoint or the spindle checkpoint. The arrest is not solely dependent upon the pachytene checkpoint that monitors recombination and aspects of chromosome synapsis. Elimination of the spindle checkpoint failed to allow kar3 mutants to undergo meiosis I nuclear division, but phenotypes of the kar3/spindle checkpoint double mutants suggest that the kar3 meiotic arrest may be mediated by the spindle checkpoint.
马达蛋白Kar3p及其相关蛋白Cik1p对于减数分裂I的进行至关重要。在缺乏这两种蛋白中的任何一种时，减数分裂细胞会停滞在前期I。进行了实验以确定这种停滞是由减数分裂过程中结构上无法进行导致的，还是由调节机制引起的。数据表明，减数分裂停滞并非结构原因导致；kar3和cik1突变体在spo11突变背景下能够形成外观正常的双极纺锤体，并将其DNA分成两团。为了确定kar3/cik1减数分裂停滞所必需的调节系统，我们测试了通过消除粗线期检查点或纺锤体检查点是否可以绕过这种停滞。这种停滞并不完全依赖于监测重组和染色体联会方面的粗线期检查点。消除纺锤体检查点未能使kar3突变体进行减数分裂I核分裂，但kar3/纺锤体检查点双突变体的表型表明，kar3减数分裂停滞可能由纺锤体检查点介导。
