Ku70 suppresses alternative end joining in G1-arrested progenitor B cells
Abstract
DNA double-strand breaks (DSBs) are repaired by two major pathways - homologous recombination and non-homologous end joining (NHEJ). Alternative end joining (alt-EJ) is a backup repair pathway that can lead to chromosomal translocations and genomic instability. This study investigates the role of Ku70, a key component of the classical NHEJ pathway, in suppressing alternative end joining in G1-arrested progenitor B cells. Using genetic and molecular approaches, we demonstrate that Ku70 plays a critical role in maintaining genomic stability by preventing the use of error-prone alt-EJ pathways during V(D)J recombination and other DSB repair processes in developing B cells.
This research provides important insights into DNA repair mechanisms in developing B cells and the role of Ku70 in preventing genomic instability. The findings have implications for understanding immune system development and cancer biology.
Lawrence Jianqiao Hu
Doctoral Candidate in Neuroscience
Ph.D. Ambassador, UW Medicine
My research interests include…