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A more recent version of this article appeared on July 1, 2006
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Submitted on November 3, 2005
Revised on March 24, 2006
Accepted on April 13, 2006

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*Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, United Kingdom;
Max Planck Institute for Terrestrial Microbiology, 35043 Marburg, Germany; ¶Clare Hall Laboratories, Cancer Research UK, South Mimms, Herts EN6 3LD, United Kingdom
Monitoring Editor: Orna Cohen-Fix
Ubiquitination of PCNA plays a crucial role in regulating replication past DNA damage in eukaryotes, but the detailed mechanisms appear to vary in different organisms. We have examined the modification of PCNA in Schizosaccharomyces pombe. We find that, in response to UV irradiation, PCNA is mono- and poly-ubiquitinated in a manner similar to that in S. cerevisiae. However in undamaged S. pombe cells, PCNA is ubiquitinated in S phase, whereas in S. cerevisiae it is sumoylated. Furthermore we find that, unlike in S. cerevisiae, mutants defective in ubiquitination of PCNA are also sensitive to ionising radiation, and PCNA is ubiquitinated following exposure of cells to ionising radiation, in a similar manner to the response to UV-irradiation. We show that PCNA modification and cell-cycle checkpoints represent two independent signals in response to DNA damage. Finally, we unexpectedly find that PCNA is ubiquitinated in response to DNA damage when cells are arrested in G2.
AbCam, Cambridge Science Park, Milton Road, Cambridge, United Kingdom; ||Marie Curie Institute, The Chart, Oxted, Surrey RH8 0TL, United Kingdom;
Heidelberg University Biochemistry Centre, 69120 Heidelberg, Germany.
Address correspondence to:
Alan R. Lehmann (a.r.lehmann{at}sussex.ac.uk)
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