Two separate studies reported in Genes & Development found that RMI2 is part of BTB complex.
Multiple research teams report the discovery of a previously unidentified fourth component of the Bloom’s syndrome (BTB) complex, an inherited cancer predisposition disease resulting from mutations in the BLM gene on the long arm of chromosome number 15.
Scientists from the National Institute on Aging and a separate group from Cincinnati Children’s Hospital Medical Center identified protein RMI2, a new OB-fold complex essential for the cellular response required to repair DNA damage.
It is known that BLM, the helicase mutated in Bloom syndrome, associates with topoisomerase 3á, RMI1, and RPA to form a complex essential for the maintenance of genome stability. Findings showed that multi-OB-fold complexes mediate two modes of BLM action: via RPA-mediated protein-DNA interaction and via RMI-mediated protein-protein interactions.
Although further research is needed to determine the precise mechanism of RMI2 action, both papers clearly posit RMI2 as an integral Bloom’s syndrome protein and protector of genome stability.
The two independent papers appear in the October 15 issue of Genes & Development.
