Human Molecular Genetics, Vol 7, 69-74, Copyright © 1998 by Oxford University Press
JK Schweitzer and DM Livingston
To understand the causes of CAG repeat tract changes that occur in the
passage of human disease alleles, we are studying the effect of replication
and repair mutations on CAG repeat tracts embedded in a yeast chromosome.
In this report, we examine the effect of a mutation in the RTH1/RAD27 gene
encoding a deoxyribonuclease needed for removal of excess nucleotides at
the 5'-end of Okazaki fragments. Deletion of the RTH1/RAD27 gene has two
effects on CAG tracts. First, the rth1/rad27 mutation destabilizes CAG
tracts. Second, although most tract length changes in wild-type yeast cells
are tract contractions, approximately half of the changes that occur as a
result of the rth1/rad27 mutation are expansions of one or more repeat
units. These results support the hypothesis that tract expansions that
occur during passage of human disease alleles bearing expanded CAG tracts
result from excess DNA synthesis on the lagging strand of replication.
ARTICLES
Expansions of CAG repeat tracts are frequent in a yeast mutant defective in Okazaki fragment maturation
Department of Biochemistry, 4-225 Millard Hall, 435 Delaware Street SE, University of Minnesota, Minneapolis, MN 55455-0347, USA.
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