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Vol. 10, Issue 9, 2905-2918, September 1999
and§
*Trescowthick Research Laboratories, Peter MacCallum Cancer
Institute, Melbourne, Victoria 8006, Australia;
To survive damage to the genome, cells must respond by activating
both DNA repair and checkpoint responses. Using genetic screens in the
fission yeast Schizosaccharomyces pombe, we recently isolated new genes required for DNA damage checkpoint control. We show
here that one of these strains defines a new allele of the previously
described rad18 gene, rad18-74. rad18 is
an essential gene, even in the absence of extrinsic DNA damage. It
encodes a conserved protein related to the structural maintenance of
chromosomes proteins. Point mutations in rad18 lead to
defective DNA repair pathways responding to both UV-induced lesions
and, as we show here, double-stranded breaks. Furthermore, rad18p is
required to maintain cell cycle arrest in the presence of DNA damage,
and failure of this leads to highly aberrant mitoses. A gene encoding a
BRCT-containing protein, brc1, was isolated as an
allele-specific high-copy suppressor of rad18-74. brc1
is required for mitotic fidelity and for cellular viability in strains
with rad18 mutations but is not essential for DNA damage
responses. Mutations in rad18 and brc1
are synthetically lethal with a topoisomerase II mutant (top2-191), indicating that these proteins play a role
in chromatin organization. These studies show a role for chromatin
organization in the maintenance or activation of responses to DNA damage.
Department of Genetics, University of Melbourne,
Parkville, Victoria 3052, Australia; and Medical
Research Council Cell Mutation Unit, Sussex University, Falmer, East
Sussex BN1 9RR, United Kingdom
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