A combination of genetic and biochemical approaches suggest that yeast Rev7 promotes DNA double-strand break repair via NHEJ and inhibits homologous recombination by blocking Mre11 nuclease and Rad50’s ATPase activities.
Bin-zhong Li, Christopher D Putnam, Richard David Kolodner
Genetic analysis combined with whole genome sequencing elucidates mechanisms and pathways that form and prevent a specific class of genome rearrangements, foldback inversions, seen in many human cancers.
p53 suppresses genome instability by direct role at stalled replication forks for pathway regulation that explains transcription-independent p53 tumor-suppressor functions.
Dorota Rousová, Vaishnavi Nivsarkar ... John R Weir
Mer2 interacts directly with meiotic chromatin, axial proteins, and the DNA break forming machinery to facilitate the formation of meiotic double-strand breaks.
Structures of the human ataxia-telangiectasia mutated (ATM) kinase alone and bound to the C-terminus of Nbs1 show the mechanisms underlying ATM autoinhibition and binding by a portion of the Mre11-Rad50-Nbs1 (MRN) activating complex.
Young Eun Choi, Yunfeng Pan ... Dipanjan Chowdhury
MicroRNAs tightly control the cellular level of homologous recombination (HR) factors in the G1 phase, and failure of this control system results in an ectopic increase in HR proteins in G1 cells leading to impaired DNA repair.
Orphan ATM kinase-domain missense mutations are unexpectedly common and form a potent oncogenic event and a biomarker for Topo-isomerase I inhibitor based therapy.
Hundreds of proteins are involved in the DNA damage response but only three sensors for DSB were known but now SIRT6 is identified as a fourth DSB sensor.
During meiosis, budding yeast use a checkpoint involving the protein Mec1 to prevent the formation of double-strand breaks in DNA that has not completed replication.
