ATR/Chk1 contribute to G2 arrest in developing tracheoblasts, and arrest in G2 facilitates cellular and hypertrophic organ growth.

Wnts can act synergistically to affect G2 arrest via transcriptional upregulation of a Checkpoint Kinase in the absence of any detectable DNA damage.

The GATOR complex regulates TORC1 activity during meiosis.

Reactive oxygen species can activate the ATR/Chk1 pathway in the absence of detectable DNA damage and without a requirement for DNA damage response proteins.

rDNA copy number is shown to dynamically change during aging and through generations, and is actively maintained in male germline of Drosophila.

Tissue damage induces a reversible cell cycle arrest in G2, which promotes survival and mitogenic signals to facilitate tissue regeneration but drives senescence-like phenotypes under chronic stress conditions.

Cell competition is an important mechanism selecting against aneuploid cells.