The activity of yeast Apn2 AP endonuclease at uracil-derived AP sites is dependent on the major carbon source.
The activity of yeast Apn2 AP endonuclease at uracil-derived AP sites is dependent on the major carbon source.
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DOI：
10.1007/s00294-020-01141-4
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发表时间：
2021-04
期刊：
影响因子：
2.5
通讯作者：
Kim N
中科院分区：
文献类型：
--
作者：
Stokdyk K;Berroyer A;Grami ZA;Kim N
酵母Apn 2是一种AP内切酶和DNA 3′-二酯酶，属于Exo III家族，与E.大肠杆菌核酸外切酶III、粟酒裂殖酵母eth 1和人AP核酸内切酶APEX 1和APEX 2。在缺乏Apn 1（酵母中主要的AP核酸内切酶）的情况下，Apn 2可以在AP损伤处切割DNA骨架，启动碱基切除修复途径。为了研究Apn 2的作用和相对贡献，我们利用了以前用于描述尿嘧啶衍生AP位点如何修复的报告系统。在这个报告者，Apn 1启动的碱基切除修复途径的中断导致A：T到C：G颠换的显著升高。在这里，我们表明，当apn 1 Δ酵母细胞在葡萄糖作为主要碳源中生长时，与DNA中尿嘧啶残基相关的这种高度升高的A：T至C：G颠换突变被消除。我们还表明，Apn 2的破坏，无论是由完整的基因缺失或催化残基的突变，结果在尿嘧啶相关的突变率同样降低。总之，我们的研究结果表明，Apn 2活性是由葡萄糖阻遏途径在酵母中调节。
Yeast Apn2 is an AP endonuclease and DNA 3′-diesterase that belongs to the Exo III family with homology to the E. coli exonuclease III, Schizosaccharomyces pombe eth1, and human AP endonucleases APEX1 and APEX2. In the absence of Apn1, the major AP endonuclease in yeast, Apn2 can cleave the DNA backbone at an AP lesion initiating the base excision repair pathway. To study the role and relative contribution of Apn2, we took advantage of a reporter system that was previously used to delineate how uracil-derived AP sites are repaired. At this reporter, disruption of the Apn1-initiated base excision repair pathway led to a significant elevation of A:T to C:G transversions. Here we show that such highly elevated A:T to C:G transversion mutations associated with uracil residues in DNA are abolished when apn1Δ yeast cells are grown in glucose as the primary carbon source. We also show that the disruption of Apn2, either by the complete gene deletion or by the mutation of a catalytic residue, results in a similarly reduced rate of the uracil-associated mutations. Overall, our results indicate that Apn2 activity is regulated by the glucose repression pathway in yeast.
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影响因子：
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作者：
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影响因子：
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作者：
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通讯作者：
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DOI：
10.1073/pnas.44.7.633
发表时间：
1958-01-01
影响因子：
11.1
作者：
BESSMAN, MJ;LEHMAN, IR;KORNBERG, A
通讯作者：
KORNBERG, A