Schär P, Kohli J
Institute of General Microbiology, University of Bern, Switzerland.
Genetics. 1993 Apr;133(4):825-35. doi: 10.1093/genetics/133.4.825.
G to C transversion mutations show very strong allele-specific marker effects on the frequency of wild-type recombinants in intragenic two-factor crosses. Here we present a detailed study of the marker effect of one representative, the ade6-M387 mutation of Schizosaccharomyces pombe. Crosses of M387 with other mutations at varying distance reveal highly increased prototroph frequencies in comparison with the C to T transition mutation ade6-51 (control without any known marker effect) located four nucleotides from M387. The marker effect of M387 is strongest (> 40-fold) for crosses with mutations less than 15 nucleotides from M387. It decreases to an intermediate level (5-10-fold) in crosses with mutations located 25-150 base pairs from M387/51 and is very low in crosses with mutations beyond 200 base pairs. On the basis of these results and the quantitation of the low efficiency of C/C mismatch repair presented in the accompanying publication we propose the existence of at least two different types of mechanisms for base mismatch repair in fission yeast. The major system is suggested to recognize all base mismatches except C/C with high efficiency and to generate long excision tracts (approximately 100 nucleotides unidirectionally). The minor system is proposed to recognize all base mismatches including C/C with low and variable efficiency and to have short excision tracts (approximately 10 nucleotides unidirectionally). We estimate from the M387 marker effect that the minor system accounts for approximately 1-8% repair of non-C/C mismatches (depending on the nature of the mutation) in fission yeast meiosis.
G到C的颠换突变在基因内双因子杂交中对野生型重组体的频率表现出非常强的等位基因特异性标记效应。在此,我们对一种代表性突变——粟酒裂殖酵母的ade6 - M387突变的标记效应进行了详细研究。将M387与不同距离处的其他突变进行杂交,结果显示与位于距M387四个核苷酸处的C到T转换突变ade6 - 51(无任何已知标记效应的对照)相比,原养型频率大幅增加。对于与距离M387小于15个核苷酸的突变进行杂交,M387的标记效应最强(>40倍)。在与距离M387/51 25 - 150个碱基对的突变进行杂交时,其标记效应降至中等水平(5 - 10倍),而在与超过200个碱基对的突变进行杂交时则非常低。基于这些结果以及随附出版物中对C/C错配修复低效率的定量分析,我们提出在裂殖酵母中至少存在两种不同类型的碱基错配修复机制。主要系统被认为能够高效识别除C/C之外的所有碱基错配,并产生长切除片段(单向约100个核苷酸)。次要系统被认为能够以低且可变的效率识别包括C/C在内的所有碱基错配,并具有短切除片段(单向约10个核苷酸)。我们根据M387的标记效应估计,次要系统在裂殖酵母减数分裂中对非C/C错配的修复约占1 - 8%(取决于突变的性质)。