RMI, a new OB-fold complex essential for Bloom syndrome protein to maintain genome stability

• DOI: 10.1101/gad.1708608
• Publication Date: 2008-10-15T17:33:18Z
• Authors: Dongyi Xu; Rong Guo; Alexandra Sobeck; Csanad Z. Bachrati; Jay Yang; Takemi Enomoto; Grant W. Brown; Maureen E. Hoatlin; Ian D. Hickson; Weidong Wang
• Keywords: Bloom syndrome; Sister chromatid exchange; RecQ helicase

BLM, the helicase mutated in Bloom syndrome, associates with topoisomerase 3α, RMI1 (RecQ-mediated genome instability), and RPA, to form a complex essential for maintenance of stability. Here we report novel component BLM complex, RMI2, which interacts through two oligonucleotide-binding (OB)-fold domains similar those RPA. The resulting named RMI, differs from RPA that it lacks obvious DNA-binding activity. Nevertheless, RMI stimulates dissolution homologous recombination intermediate vitro is stability, localization, function vivo. Notably, inactivation RMI2 chicken DT40 cells results an increased level sister chromatid exchange (SCE)—the hallmark feature syndrome cells. Epistasis analysis revealed suppress SCE within same pathway. A point mutation OB domain disrupts association between rest abrogates ability elevated SCE. Our data suggest multi-OB-fold complexes mediate modes action: via RPA-mediated protein–DNA interaction, RMI-mediated protein–protein interactions.