Unspliced tRNAs (green) accumulate in the nucleus in response to DNA damage (right).

GHADIVEL/ELSEVIER

Shutting down nuclear export of unspliced tRNA keeps cells in G1 during DNA repair, say Ata Ghavidel and colleagues (University of Toronto, Canada).

The authors found that DNA damage caused the nuclear accumulation of tRNAs containing unspliced introns, which are removed in the cytoplasm. This accumulation required the damage-induced signaling molecule Rad53 and correlated with the retention of the main tRNA export receptor, Los1, in the cytoplasm.

Without their exporter, tRNAs were stuck in the nucleus, causing cell cycle arrest in G1 and giving the cell time to repair damage before DNA synthesis. Deleting Rad53 prevented the nuclear tRNA build-up, and damaged cells exited G1 prematurely. Deleting Los1 in these cells restored the G1 arrest.

The G1 stall was not due to decreased cytoplasmic tRNA, which remained in large excess due...

You do not currently have access to this content.