Saccharomyces cerevisiae pol30 (proliferating cell nuclear antigen) mutations impair replication fidelity and mismatch repair.
Saccharomyces cerevisiae pol30 (proliferating cell nuclear antigen) mutations impair replication fidelity and mismatch repair.
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酿酒酵母 pol30（增殖细胞核抗原）突变会损害复制保真度和错配修复。
DOI：
10.1128/mcb.19.11.7801
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发表时间：
1999
影响因子：
5.3
通讯作者：
Kolodner,RD
中科院分区：
文献类型：
--
作者：
Chen,C;Merrill,BJ;Lau,PJ;Holm,C;Kolodner,RD
为了了解POL 30在突变抑制中的作用，对11株酿酒酵母POL 30突变体进行了表征。这些突变体根据其致突变缺陷进行分组。许多pol 30突变体具有多个致突变缺陷，并被置于多个组中。A组突变（pol 30 -52、-104、-108和-126）导致错配修复（MMR）缺陷。这些突变体表现出的突变率和光谱让人联想到MMR缺陷型突变体，并在体内MMR测定中有缺陷。amsh 2和amsh 6突变可提高A组突变体的突变率，表明MMR缺陷不是唯一的致突变缺陷。组B突变体（pol 30 -45、-103、-105、-126和-114）表现出增加的单独缺失或缺失和重复的组合（4至60 bp）的积累。所有缺失和重复断裂点的侧翼都有3 - 7 bp的不完全同向重复序列。对一个代表性的B组突变体pol 30 -126的遗传分析表明，聚合酶滑移是可能的致突变机制。C组突变体（pol 30 -100、-103、-105、-108和-114）积累碱基替换，当与msh 6突变组合时，突变率显示协同增加，表明DNA聚合酶错误掺入增加是致突变缺陷。MSH 2的失活几乎完全抑制了A组突变体pol 30 -104和rad 52之间的合成致死性。此外，pol 30 - 104引起的超重组表型被amsh 2突变部分抑制。这些结果表明pol 30 - 104菌株以MSH 2依赖的方式积累DNA断裂。
To understand the role ofPOL30in mutation suppression, 11Saccharomyces cerevisiae pol30mutator mutants were characterized. These mutants were grouped based on their mutagenic defects. Manypol30mutants harbor multiple mutagenic defects and were placed in more than one group. Group A mutations (pol30-52, -104, -108, and -126) caused defects in mismatch repair (MMR). These mutants exhibited mutation rates and spectra reminiscent of MMR-defective mutants and were defective in an in vivo MMR assay. The mutation rates of group A mutants were enhanced by amsh2or amsh6mutation, indicating that MMR deficiency is not the only mutagenic defect present. Group B mutants (pol30-45, -103, -105, -126, and -114) exhibited increased accumulation of either deletions alone or a combination of deletions and duplications (4 to 60 bp). All deletion and duplication breakpoints were flanked by 3 to 7 bp of imperfect direct repeats. Genetic analysis of one representative group B mutant,pol30-126, suggested polymerase slippage as the likely mutagenic mechanism. Group C mutants (pol30-100, -103, -105, -108, and -114) accumulated base substitutions and exhibited synergistic increases in mutation rate when combined withmsh6mutations, suggesting increased DNA polymerase misincorporation as a mutagenic defect. The synthetic lethality between a group A mutant,pol30-104, andrad52was almost completely suppressed by the inactivation ofMSH2. Moreover,pol30-104caused a hyperrecombination phenotype that was partially suppressed by amsh2mutation. These results suggest thatpol30-104strains accumulate DNA breaks in aMSH2-dependent manner.
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影响因子：
16
作者：
Chen, C;Umezu, K;Kolodner, RD
通讯作者：
Kolodner, RD
RAD52 重组修复途径对于 pol30 (PCNA) 突变体至关重要，该突变体在 DNA 合成过程中积累小的单链 DNA 片段。
影响因子：
3.3
作者：
Merrill,BJ;Holm,C
通讯作者：
Holm,C
DOI：
10.1073/pnas.95.21.12404
发表时间：
1998-10-13
影响因子：
11.1
作者：
Flores-Rozas, H;Kolodner, RD
通讯作者：
Kolodner, RD
影响因子：
3.6
作者：
Matsiukevich, Dzmitry;House, Stacey L.;Weinheimer, Carla;Kovacs, Attila;Ornitz, David M.
通讯作者：
Ornitz, David M.
影响因子：
13.8
作者：
Kelman, Z;Hurwitz, J
通讯作者：
Hurwitz, J