The RAD52 recombinational repair pathway is essential in pol30 (PCNA) mutants that accumulate small single-stranded DNA fragments during DNA synthesis.
The RAD52 recombinational repair pathway is essential in pol30 (PCNA) mutants that accumulate small single-stranded DNA fragments during DNA synthesis.
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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。
DOI：
10.1093/genetics/148.2.611
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发表时间：
1998
期刊：
影响因子：
3.3
通讯作者：
Holm,C
中科院分区：
文献类型：
--
作者：
Merrill,BJ;Holm,C
为了鉴定补偿受损的增殖细胞核抗原（酵母中的PCNA或Pol 30 p）活性的体内途径，我们用酵母pol 30 -104突变进行了合成致死筛选。我们确定了9个突变，显示与pol 30 -104的合成致死性; 3个突变影响复制因子C大亚基（rfc 1）的结构基因，其将PCNA加载到DNA上，6个突变影响了3个成员的RAD 52上位组的DNA重组修复（rad 50，rad 52和rad 57）。我们还发现，pol 30 -104显示出合成致死性，其在RAD 52上位性组的其他成员（rad 51和rad 54）中具有突变，但在RAD 3和RAD 6上位性组的成员中不具有突变。对9种不同的pol 30突变的分析表明，对RAD 52途径的需求与DNA复制缺陷相关，但与pol 30突变引起的相对DNA修复缺陷无关。此外，需要RAD 52来维持活力的突变体（pol 30 -100、pol 30 -104、rfc 1 -1和rth 1 Δ）在体内DNA复制期间积累小的单链DNA片段。综上所述，这些数据表明，当冈崎片段的成熟存在缺陷时，需要RAD 52途径。
To identify in vivo pathways that compensate for impaired proliferating cell nuclear antigen (PCNA or Pol30p in yeast) activity, we performed a synthetic lethal screen with the yeast pol30-104 mutation. We identified nine mutations that display synthetic lethality with pol30-104; three mutations affected the structural gene for the large subunit of replication factor C (rfc1), which loads PCNA onto DNA, and six mutations affected three members of the RAD52 epistasis group for DNA recombinational repair (rad50, rad52, and rad57). We also found that pol30-104 displayed synthetic lethality with mutations in other members of the RAD52 epistasis group (rad51 and rad54), but not with mutations in members of the RAD3 nor the RAD6 epistasis group. Analysis of nine different pol30 mutations shows that the requirement for the RAD52 pathway is correlated with a DNA replication defect but not with the relative DNA repair defect caused by pol30 mutations. In addition, mutants that require RAD52 for viability (pol30-100, pol30-104, rfc1-1 and rth1Δ) accumulate small single-stranded DNA fragments during DNA replication in vivo. Taken together, these data suggest that the RAD52 pathway is required when there are defects in the maturation of Okazaki fragments.