The photolyases PHR1 and PHR2 enable photorepair of fungal DNA lesions in the forms of UV-induced cyclobutane pyrimidine dimer (CPD) and (6-4)-pyrimidine-pyrimidone (6-4PP) photoproducts, but their regulation remains mechanistically elusive. Here, we report that the white collar proteins WC1 and WC2 mutually interacting to form a light-responsive transcription factor regulate photolyase expression required for fungal UV resistance in the insect-pathogenic fungus Metharhizum robertsii. Conidial UVB resistance decreased by 54% in Δwc1 and 67% in Δwc2. Five-hour exposure of UVB-inactivated conidia to visible light resulted in photoreactivation rates of 30% and 9% for the Δwc1 and Δwc2 mutants, contrasting to 79%–82% for wild-type and complemented strains. Importantly, abolished transcription of phr1 in Δwc-2 and of phr2 in Δwc1 resulted in incapable photorepair of CDP and 6-4PP DNA lesions in UVB-impaired Δwc2 and Δwc1 cells respectively. Yeast two-hybrid assays revealed interactions of either WC protein with both PHR1 and PHR2. Therefore, the essential roles for WC1 and WC2 in both photorepair of UVB-induced DNA lesions and photoreactivation of UVB-inactivated conidia rely upon their interactions with, and hence transcriptional activation of, PHR1 and PHR2. These findings uncover a novel WC-cored pathway that mediates filamentous fungal response and adaptation to solar UV irradiation.

中文翻译：

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两种白领蛋白通过与绿僵菌中的两种光解酶相互作用来保护真菌细胞免受太阳紫外线的伤害

光解酶 PHR1 和 PHR2 能够以紫外线诱导的环丁烷嘧啶二聚体 (CPD) 和 (6-4)-嘧啶-嘧啶酮 (6-4PP) 光产物的形式对真菌 DNA 损伤进行光修复，但它们的调节机制仍然难以捉摸。在这里，我们报告白领蛋白 WC1 和 WC2 相互作用形成光响应转录因子调节昆虫病原真菌Metharhizum robertsii中真菌抗紫外线所需的光解酶表达。分生孢子 UVB 抗性在 Δ wc1中下降了 54%，在 Δ wc2中下降了67% 。将 UVB 灭活的分生孢子暴露于可见光 5 小时导致 Δwc1 和 Δwc2 的光活化率分别为 30%和9 %突变体，而野生型和互补菌株的比例为 79%–82%。重要的是，Δ wc-2中phr1和 Δ wc1中phr2的转录被取消，导致 UVB 受损的 Δ wc2和 Δ wc1中的 CDP 和 6-4PP DNA 损伤无法进行光修复细胞分别。酵母双杂交试验揭示了任一 WC 蛋白与 PHR1 和 PHR2 的相互作用。因此，WC1 和 WC2 在 UVB 诱导的 DNA 损伤的光修复和 UVB 灭活的分生孢子的光激活中的重要作用依赖于它们与 PHR1 和 PHR2 的相互作用，从而转录激活。这些发现揭示了一种新的以 WC 为核心的途径，该途径介导丝状真菌对太阳紫外线照射的反应和适应。