Monopolar spindle 1 (MPS1) protein-dependent phosphorylation of RecQ-mediated genome instability protein 2 (RMI2) at serine 112 is essential for BLM-Topo III α-RMI1-RMI2 (BTR) protein complex function upon spindle assembly checkpoint (SAC) activation during mitosis.

ABSTRACT: Genomic instability and a predisposition to cancer are hallmarks of Bloom syndrome, an autosomal recessive disease arising from mutations in the BLM gene. BLM is a RecQ helicase component of the BLM-Topo III α-RMI1-RMI2 (BTR) complex, which maintains chromosome stability at the spindle assembly checkpoint (SAC). Other members of the BTR complex include Topo IIIa, RMI1, and RMI2. All members of the BTR complex are essential for maintaining the stable genome. Interestingly, the BTR complex is posttranslationally modified upon SAC activation during mitosis, but its significance remains unknown. In this study, we show that two proteins that interact with BLM, RMI1 and RMI2, are phosphorylated upon SAC activation, and, like BLM, RMI1, and RMI2, are phosphorylated in an MPS1-dependent manner. An

SUBMITTER: Pradhan A 

PROVIDER: S-EPMC3837099 | biostudies-literature | 2013 Nov

REPOSITORIES: biostudies-literature