Given that capping protects telomeres from repair and checkpoint activation, it seemed logical to think that proteins involved in DNA repair and checkpoints would not act at telomeres.
Relying on the aforementioned biological evidences, and focusing on the inclusion of senescence as an additional outcome of the checkpoint arrest, we delineate a logical version of the regulation of the G1/S checkpoint.
In summary, we have defined a precursory logical model for the G1/S checkpoint where ATR and ATM pathways activation by single and double DNA strand breaks is sufficient to determine three different cell fates: cell cycle arrest, apoptosis and senescence.
We derived the logical properties to check from essential checkpoint conditions of the budding yeast cell cycle.
It would be logical for diseased cells to have a checkpoint to safeguard against proliferation of defective mitochondria.
Searching the literature and partly building on the network of human G1/S checkpoint activation [ 2], we propose a logical model of cell fate decision upon DNA damage, including proliferation, transient arrest for DNA repair, apoptosis and, notably, senescence.
The logical first step is to better screen women at key security checkpoints.
In an attempt to predict the trends in phenotypic variation that we might observe in the tetraploid mutant series, we constructed a logical model of the S.cerevisiae cell cycle and simulated the effects of deleting the HFC G2/M checkpoint genes.
Liberty Street would seem to be the logical place, except that westbound lanes would conflict with eastbound trucks bound for a ramp to the security checkpoints and delivery bays that are planned underground.
Checkpoints proliferated.
