ATR protects stem cell genomes by activating a transcriptional response mediated by totipotency genes, conferring trophoblast differentiation potential, the derepression of which in somatic cells might favour cancer features emergence.

Evolutionary adaptation to a constitutive perturbation of DNA replication reveals that adaptive mutations in three conserved pathways interact to restore faithful chromosome replication and segregation.

The RIF1-long and short splice variants show distinct ability to protect cells from replication stress by promoting 53BP1 nuclear bodies, representing the first described functional difference between the two variants.

During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.

Retrograde signaling activates the Rad53 checkpoint kinase independently of the canonical DNA replication stress response.

Mutation of Glycine 34 to Arginine within the N-terminal tail of histone H3 alters post-translational modifications on Lysine 36 and is associated with a delay in replication restart, defective homologous recombination and an increase in genomic instability.

Nucleosomal DNAs assembled or modified by different chromatin remodeling enzymes differentially impact the origin licensing and helicase activation steps of replication initiation.

The localization of Rad53 cell cycle checkpoint kinase to many gene promoters and the dynamic changes in response to replication stress suggests that the kinase may coordinate genome stability and gene expression.

Translesion polymerase kappa promotes replication fork restart to maintain genome stability during conditions of nucleotide deprivation.

Small molecule inhibitors identified in a biophysical high-throughout screening assay confirm the importance of the interaction between single-stranded DNA and the protein RAD52 for the survival of BRCA2-depleted cells.