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First published online 25 November 2008
doi: 10.1242/jcs.035428

Journal of Cell Science 121, 4047-4054 (2008)
Published by The Company of Biologists 2008
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Research Article

The G1-S checkpoint in fission yeast is not a general DNA damage checkpoint

Marit Krohn*, Henriette C. Skjølberg*, Héla Soltani, Beáta Grallert and Erik Boye{ddagger}

Department of Cell Biology, Institute for Cancer Research, Rikshospitalet Medical Centre, Montebello, 0310 Oslo, Norway

{ddagger} Author for correspondence (e-mail: eboye{at}rr-research.no)

Accepted 10 September 2008

Inhibitory mechanisms called checkpoints regulate progression of the cell cycle in the presence of DNA damage or when a previous cell-cycle event is not finished. In fission yeast exposed to ultraviolet light the G1-S transition is regulated by a novel checkpoint that depends on the Gcn2 kinase. The molecular mechanisms involved in checkpoint induction and maintenance are not known. Here we characterise the checkpoint further by exposing the cells to a variety of DNA-damaging agents. Exposure to methyl methane sulphonate and hydrogen peroxide induce phosphorylation of eIF2{alpha}, a known Gcn2 target, and an arrest in G1 phase. By contrast, exposure to psoralen plus long-wavelength ultraviolet light, inducing DNA adducts and crosslinks, or to ionizing radiation induce neither eIF2{alpha} phosphorylation nor a cell-cycle delay. We conclude that the G1-S checkpoint is not a general DNA-damage checkpoint, in contrast to the one operating at the G2-M transition. The tight correlation between eIF2{alpha} phosphorylation and the presence of a G1-phase delay suggests that eIF2{alpha} phosphorylation is required for checkpoint induction. The implications for checkpoint signalling are discussed.

Key words: Checkpoint, DNA replication, Cell cycle, DNA damage, G1 phase, eIF2{alpha}, Fission yeast


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