Sugahara Ryohei, Mon Hiroaki, Lee Jae Man, Shiotsuki Takahiro, Kusakabe Takahiro
Laboratory of Silkworm Science, Kyushu University Graduate School of Bioresource and Bioenvironmental Sciences, 6-10-1 Hakozaki, Fukuoka 812-8581, Japan; Insect Growth Regulation Research Unit, National Institute of Agrobiological Sciences, 1-2 Owashi, Tsukuba, Ibaraki 305-8634, Japan.
Laboratory of Silkworm Science, Kyushu University Graduate School of Bioresource and Bioenvironmental Sciences, 6-10-1 Hakozaki, Fukuoka 812-8581, Japan.
FEBS Lett. 2014 Nov 3;588(21):3959-63. doi: 10.1016/j.febslet.2014.09.009. Epub 2014 Sep 19.
The silkworm Fanconi anemia (FA) pathway is required for normal cellular resistance to mitomycin C (MMC) in silkworms, but little is known about the requirement for repair of other types of DNA damage. Here we report that silkworm cells deficient for FA proteins FancD2 and FancM exhibit normal sensitivities to hydroxyurea (HU) and camptothecin (CPT), although FancM-dependent FancD2 monoubiquitination is induced upon these treatments. Similar results were observed in cells depleted for Rmi1 and Mhf1, which interact with the FancM protein. We also found that Rad51-knockdown cells exhibited normal sensitivity to HU despite induction of double-strand breaks by HU treatment.
家蚕范可尼贫血（FA）途径是家蚕细胞对丝裂霉素C（MMC）产生正常细胞抗性所必需的，但对于修复其他类型DNA损伤的需求了解甚少。在此我们报告，缺乏FA蛋白FancD2和FancM的家蚕细胞对羟基脲（HU）和喜树碱（CPT）表现出正常的敏感性，尽管在这些处理后会诱导FancM依赖的FancD2单泛素化。在与FancM蛋白相互作用的Rmi1和Mhf1缺失的细胞中也观察到了类似结果。我们还发现，尽管HU处理会诱导双链断裂，但Rad51敲低细胞对HU仍表现出正常的敏感性。
