Epigenetic restriction of herpes simplex virus occurs in a biphasic manner, in which ATRX maintains viral heterochromatin after an initial phase of chromatin deposition.
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.
ATM plays an important role in maintaining the fidelity of DNA repair through the regulation of ARP8 phosphorylation to prevent the chromosome abnormality.
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.
ChIP-seq and phenotypic analyses reveal Atrophin from Drosophila directly regulates Notch and Dpp signaling components, and engrailed gene expression, via interactions with GAGA Factor.
The conversion of the ends of a double-strand break from double-stranded to single-stranded DNA, which is necessary to initiate homologous recombination, is responsible for loss of transcription and RNA polymerase occupancy around the double-strand break in Saccharomyces cerevisiae.
Two phosphorylation sites on 53BP1 are found to mediate interaction with TOPBP1-RAD9 and shown to be essential for assembling the G1 DNA damage checkpoint response apparatus.
