Bailis J M, Smith A V, Roeder G S
Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT 06520-8103, USA.
Mol Cell Biol. 2000 Jul;20(13):4838-48. doi: 10.1128/MCB.20.13.4838-4848.2000.
The Saccharomyces cerevisiae zip1 mutant, which exhibits defects in synaptonemal complex formation and meiotic recombination, triggers a checkpoint that causes cells to arrest at the pachytene stage of meiotic prophase. Overproduction of either the meiotic chromosomal protein Red1 or the meiotic kinase Mek1 bypasses this checkpoint, allowing zip1 cells to sporulate. Red1 or Mek1 overproduction also promotes sporulation of other mutants (zip2, dmc1, hop2) that undergo checkpoint-mediated arrest at pachytene. In addition, Red1 overproduction antagonizes interhomolog interactions in the zip1 mutant, substantially decreasing double-strand break formation, meiotic recombination, and homologous chromosome pairing. Mek1 overproduction, in contrast, suppresses checkpoint-induced arrest without significantly decreasing meiotic recombination. Cooverproduction of Red1 and Mek1 fails to bypass the checkpoint; moreover, overproduction of the meiotic chromosomal protein Hop1 blocks the Red1 and Mek1 overproduction phenotypes. These results suggest that meiotic chromosomal proteins function in the signaling of meiotic prophase defects and that the correct stoichiometry of Red1, Mek1, and Hop1 is needed to achieve checkpoint-mediated cell cycle arrest at pachytene.
酿酒酵母zip1突变体在联会复合体形成和减数分裂重组过程中表现出缺陷，它会触发一个检查点，导致细胞在减数分裂前期的粗线期停滞。减数分裂染色体蛋白Red1或减数分裂激酶Mek1的过量表达绕过了这个检查点，使zip1细胞能够形成孢子。Red1或Mek1的过量表达也促进了其他在粗线期因检查点介导而停滞的突变体（zip2、dmc1、hop2）形成孢子。此外，Red1的过量表达拮抗了zip1突变体中的同源染色体间相互作用，显著减少了双链断裂的形成、减数分裂重组和同源染色体配对。相比之下，Mek1的过量表达抑制了检查点诱导的停滞，而不会显著减少减数分裂重组。Red1和Mek1的共同过量表达未能绕过检查点；此外，减数分裂染色体蛋白Hop1的过量表达阻断了Red1和Mek1过量表达的表型。这些结果表明，减数分裂染色体蛋白在减数分裂前期缺陷的信号传导中起作用，并且需要Red1、Mek1和Hop1的正确化学计量比来实现检查点介导的细胞周期在粗线期的停滞。
