Volume 17 Issue 6, June 2016

The long non-coding RNA LINP1 facilitates double-strand break repair in triple-negative breast cancer through non-homologous end joining, by recruiting DNA-PKcs to sites of damage.

The Fanconi anaemia DNA repair pathway also has cytoplasmic functions in selective autophagy that might contribute to Fanconi anaemia disease.

Three studies provide important insights into mitochondrial function during ageing — they reveal a connection to stem cell senescence and shed light on the epigenetic mechanisms underlying UPR^mtactivation and stress-induced longevity.

DNA supercoiling and the formation of loops suppresses the ATR checkpoint and is required for proper replication of centromeric DNA.

As far as James Haber is concerned, the big picture is all he wants of protein structures. This was not the case, however, with the structure of RecA, published in 2008.

Microtubule detyrosination is shown to influence mechanical properties of cardiomyocytes, as detyrosinated microtubules resist the force of contraction by undergoing buckling.

Tomas Lindahl presents a case for keeping DNA in the organic solvent glycol, in which it keeps its activity and is better protected from contamination and, potentially, radiation.

Proteins of the Fanconi anaemia pathway are master regulators of genomic integrity through their interactions with other DNA repair pathways to repair interstrand crosslinks, stabilize replication forks and regulate cytokinesis.

Ribonucleotides are incorporated into DNA by various mechanisms, including by DNA polymerases during replication. Such ribonucleotides may have physiological functions, but their presence is typically associated with diverse structural aberrations and interferes with fundamental processes, including DNA replication, repair and transcription. Thus, efficient mechanisms of ribonucleotide removal are key to maintaining genomic integrity and functionality.

Double-strand break (DSB) repair at telomeres — the ends of linear chromosomes — can cause chromosome end fusions and genomic instability, which drives tumorigenesis. As several mechanisms protect mammalian telomeres from the DNA damage response, telomeres have emerged as a system to uncover key steps in DSB repair.

Signalling by ubiquitin, SUMO and other ubiquitin-like modifiers (UBLs), and crosstalk between these modifications, underlies cellular responses to DNA double-strand breaks (DSBs). Important insights have been gained into the mechanisms by which ubiquitin and UBLs regulate protein interactions at DSB sites to enable accurate repair in mammalian cells, thereby protecting genome integrity.