Bhargava J, Engebrecht J, Roeder G S
Department of Biology, Yale University, New Haven, Connecticut 06511-8112.
Genetics. 1992 Jan;130(1):59-69. doi: 10.1093/genetics/130.1.59.
A mutation at the REC102 locus was identified in a screen for yeast mutants that produce inviable spores. rec102 spore lethality is rescued by a spo13 mutation, which causes cells to bypass the meiosis I division. The rec102 mutation completely eliminates meiotically induced gene conversion and crossing over but has no effect on mitotic recombination frequencies. Cytological studies indicate that the rec102 mutant makes axial elements (precursors to the synaptonemal complex), but homologous chromosomes fail to synapse. In addition, meiotic chromosome segregation is significantly delayed in rec102 strains. Studies of double and triple mutants indicate that the REC102 protein acts before the RAD52 gene product in the meiotic recombination pathway. The REC102 gene was cloned based on complementation of the mutant defect and the gene was mapped to chromosome XII between CDC25 and STE11.
在一项针对产生不可育孢子的酵母突变体的筛选中，鉴定出了REC102位点的一个突变。rec102孢子致死性可被spo13突变挽救，spo13突变使细胞绕过减数分裂I期。rec102突变完全消除了减数分裂诱导的基因转换和交叉，但对有丝分裂重组频率没有影响。细胞学研究表明，rec102突变体形成轴向元件（联会复合体的前体），但同源染色体未能联会。此外，rec102菌株中减数分裂染色体分离显著延迟。对双突变体和三突变体的研究表明，REC102蛋白在减数分裂重组途径中作用于RAD52基因产物之前。基于对突变缺陷的互补作用克隆了REC102基因，并将该基因定位到XII号染色体上CDC25和STE11之间。
