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首页> 外文期刊>Molecular and Cellular Biology >Yeast RAD26, a Homolog of the Human CSB Gene, Functions Independently of Nucleotide Excision Repair and Base Excision Repair in Promoting Transcription through Damaged Bases
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Yeast RAD26, a Homolog of the Human CSB Gene, Functions Independently of Nucleotide Excision Repair and Base Excision Repair in Promoting Transcription through Damaged Bases

机译：酵母RAD26是人类CSB基因的同源物，其功能独立于核苷酸切除修复和碱基切除修复，以通过受损碱基促进转录。

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摘要

RAD26 in the yeast Saccharomyces cerevisiae is the counterpart of the human Cockayne syndrome group B (CSB) gene. Both RAD26 and CSB act in the preferential repair of UV lesions on the transcribed strand, and in this process, they function together with the components of nucleotide excision repair (NER). Here, we examine the role of RAD26 in the repair of DNA lesions induced upon treatment with the alkylating agent methyl methanesulfonate (MMS). MMS-induced DNA lesions include base damages such as 3-methyl adenine and 7-methyl guanine, and these lesions are removed in yeast by the alternate competing pathways of base excision repair (BER), which is initiated by the action of MAG1-encoded N-methyl purine DNA glycosylase, and NER. Interestingly, a synergistic increase in MMS sensitivity was observed in the rad26Δ strain upon inactivation of NER or BER, indicating that RAD26 promotes the survival of MMS-treated cells by a mechanism that acts independently of either of these repair pathways. The galactose-inducible transcription of the GAL2, GAL7, and GAL10 genes is reduced in MMS-treated rad26Δ cells and also in mag1Δ rad14Δ cells, whereas a very severe reduction in transcription occurs in MMS-treated mag1Δ rad14Δ rad26Δ cells. From these observations, we infer that RAD26 plays a role in promoting transcription by RNA polymerase II through damaged bases. The implications of these observations are discussed in this paper.
机译：酵母中的 RAD26 是人类Cockayne综合征B组（ CSB ）基因的对应物。 RAD26 和 CSB 都在转录链上紫外线损伤的优先修复中起作用，在此过程中，它们与核苷酸切除修复（NER）的成分一起发挥作用。在这里，我们检查了 RAD26 在修复烷基化剂甲磺酸甲酯（MMS）处理后诱导的DNA损伤中的作用。 MMS诱导的DNA损伤包括碱基损伤，例如3-甲基腺嘌呤和7-甲基鸟嘌呤，并且这些损伤通过碱基切除修复（BER）的交替竞争途径在酵母中被清除，这是由的作用引发的MAG1 编码的 N -甲基嘌呤DNA糖基化酶和NER。有趣的是，在NER或BER失活后，在 rad26 Δ菌株中观察到MMS协同增效，表明 RAD26 通过一种机制促进MMS处理细胞的存活。与这些修复路径中的任何一个无关地起作用。在MMS处理的 rad26 Δ中， GAL2 ， GAL7 和 GAL10 基因的半乳糖诱导转录降低细胞以及 mag1 Δ rad14 Δ细胞中，而在MMS处理的 mag1 Δ rad14 < / em>Δ rad26 Δ个细胞。从这些观察结果，我们推断 RAD26 在促进RNA聚合酶II通过受损碱基的转录中发挥作用。本文讨论了这些观察结果的含义。

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