DNA damage control

Radiation track and DNA damage

Control of G1 arrest after DNA damage.

The temporal relationship between DNA damage and DNA replication may be critical in determining whether the genetic changes necessary for cellular transformation occur after DNA damage. Recent characterization of the mechanisms responsible for alterations in cell-cycle progression after DNA damage in our laboratory have implicated the p53 (tumor suppressor) protein in the G1 arrest that occurs ...

The yeast DNA damage checkpoint proteins control a cytoplasmic response to DNA damage.

A single HO endonuclease-induced double-strand break (DSB) is sufficient to activate the DNA damage checkpoint and cause Saccharomyces cells to arrest at G(2)/M for 12-14 h, after which cells adapt to the presence of the DSB and resume cell cycle progression. The checkpoint signal leading to G(2)/M arrest was previously shown to be nuclear-limited. Cells lacking ATR-like Mec1 exhibit no DSB-ind...

DNA-damage response control of E2F7 and E2F8.

Here, we report that the two recently identified E2F subunits, E2F7 and E2F8, are induced in cells treated with DNA-damaging agents where they have an important role in dictating the outcome of the DNA-damage response. The DNA-damage-dependent induction coincides with the binding of E2F7 and E2F8 to the promoters of certain E2F-responsive genes, most notably that of the E2F1 gene, in which E2F7...

DNA-Damage Control: Claspin Destruction Turns off the Checkpoint

The ATR-Claspin-Chk1 pathway is critical for turning on the cellular response to DNA damage and replication stress. Five recent reports uncover new mechanisms controlling the recovery phase of the checkpoint response, and introduce crucial roles for Claspin, Rad17 phosphorylation and the ubiquitin proteasome pathway in Chk1 signaling.