作者: R. Sugahara , H. Mon , J. M. Lee , T. Kusakabe
DOI: 10.1111/IMB.12072
关键词: FANCM 、 FANCA 、 DNA 、 DNA repair 、 Genetics 、 Biology 、 Protein subunit 、 FANCD2 、 Monoubiquitination 、 RMI1
摘要: The Fanconi anaemia (FA) pathway is responsible for interstrand crosslink (ICL) repair. Among the FA core complex components, FANCM believed to act as a damage sensor ICL-blocked replication fork and also molecular platform assembly interaction with Bloom's syndrome (BS) that thought play an important role in processing of DNA structures such stalled forks. In present study, we found silkworms, Bombyx mori, species lacking major components (FANCA, B, C, E, F, G), FancM required FancD2 monoubiquitination cell proliferation presence mitomycin C (MMC). Silkworm (BmFancM) was phosphorylated middle regions, modification associated its subcellular localization. addition, BmFancM interacted Mhf1, histone-fold protein, Rmi1, subunit BS complex, different regions. region containing at least these two protein-binding domains played essential FancM-dependent resistance MMC. Our results suggest acts recruitment both protein although silkworm genome seems lose FAAP24, FancM-binding partner mammals.