SLX4 is a scaffold to coordinate the action of structure-specific endonucleases that are required for homologous recombination and DNA repair. In view of ScSLX4 functions in the maintenance and stability of the genome in Saccharomyces cerevisiae, we have explored the roles of CaSLX4 in Candida albicans. Here, we constructed slx4Δ/Δ mutant and found that it exhibited increased sensitivity to the DNA damaging agent, methyl methanesulfonate (MMS) but not the DNA replication inhibitor, hydroxyurea (HU). Accordingly, RT-qPCR and western blotting analysis revealed the activation of SLX4 expression in response to MMS. The deletion of SLX4 resulted in a defect in the recovery from MMS-induced filamentation to yeast form and re-entry into the cell cycle. Like many other DNA repair genes, SLX4 expression was activated by the checkpoint kinase Rad53 under MMS-induced DNA damage. In addition, SLX4 was not required for the inactivation of the DNA damage checkpoint, as indicated by normal phosphorylation of Rad53 in slx4Δ/Δ cells. Therefore, our results demonstrate SLX4 plays an important role in cell recovery from MMS-induced DNA damage in C. albicans.

中文翻译：

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从 MMS 诱导的白色念珠菌 DNA 损伤中恢复细胞需要酿酒酵母 SLX4 的同源物

SLX4 是一种支架，可协调同源重组和 DNA 修复所需的结构特异性核酸内切酶的作用。鉴于 ScSLX4 在 Saccharomyces cerevisiae 基因组的维持和稳定性中的作用，我们探索了 CaSLX4 在白色念珠菌中的作用。在这里，我们构建了 slx4Δ/Δ 突变体，发现它对 DNA 损伤剂甲磺酸甲酯 (MMS) 的敏感性增加，但对 DNA 复制抑制剂羟基脲 (HU) 没有。因此，RT-qPCR 和蛋白质印迹分析揭示了响应 MMS 的 SLX4 表达的激活。SLX4 的缺失导致从 MMS 诱导的丝状化恢复为酵母形式并重新进入细胞周期的缺陷。像许多其他 DNA 修复基因一样，SLX4 表达被 MMS 诱导的 DNA 损伤下的检查点激酶 Rad53 激活。此外，如 slx4Δ/Δ 细胞中 Rad53 的正常磷酸化所示，DNA 损伤检查点的失活不需要 SLX4。因此，我们的结果表明 SLX4 在从 MMS 诱导的白色念珠菌 DNA 损伤中恢复细胞中起重要作用。