DNA Double-Strand Breaks

DNA Double-Strand Breaks

The activation-induced cytidine deaminase (AID) is required for somatic hypermutation (SHM) and class-switch recombination (CSR) of immunoglobulin (Ig) genes, both of which are associated with DNA double-strand breaks (DSBs). As AID is capable of deaminating deoxy-cytidine (dC) to deoxy-uracil (dU), it might induce nicks (single strand DNA breaks) and also DNA DSBs via a U-DNA glycosylase-media...

DNA Double-Strand Breaks Relieve

DNA Double-Strand Breaks Come into Focus

The Mre11-Rad50-Nbs1 (MRN) complex senses DNA double-strand breaks and recruits different repair pathway and checkpoint proteins to break foci. Two new studies (Williams et al., 2009; Lloyd et al., 2009) identify Nbs1 as a key factor in this process and reveal how an N-terminal protein recruitment module in Nbs1 binds to different response factors through shared phosphopeptide motifs.

Chromatin Remodeling at DNA Double-Strand Breaks

DNA double-strand breaks (DSBs) can arise from multiple sources, including exposure to ionizing radiation. The repair of DSBs involves both posttranslational modification of nucleosomes and concentration of DNA-repair proteins at the site of damage. Consequently, nucleosome packing and chromatin architecture surrounding the DSB may limit the ability of the DNA-damage response to access and repa...

Nucleolar responses to DNA double-strand breaks

Maintenance of cellular homeostasis is key to prevent transformation and disease. The cellular response to DNA double-strand breaks, primarily orchestrated by the ATM/ATR kinases is one of many mechanisms that serve to uphold genome stability and homeostasis. Upon detection of double-strand breaks (DSBs), several signaling cascades are activated to halt cell cycle progression and initiate repai...