Nucleic Acids Research, 2001, Vol. 29, No. 14 3080-3086
© 2001 Oxford University Press
Deletion of the CSB homolog, RAD26, yields Spt– strains with proficient transcription-coupled repair
Laboratory for Cancer Research, Rutgers, The State University of New Jersey, 164 Frelinghuysen Road, Piscataway, NJ 08854-8020, USA
It has been previously shown that disruption of RAD26 in yeast strain W303-1B results in a strain that is deficient in transcription-coupled repair (TCR), the preferential repair of the transcribed strand of an expressed gene over the non-transcribed strand and the rest of the genome. RAD26 encodes a protein that is homologous to Cockayne syndrome group B protein (CSB) and is a member of the SWI2/SNF2 family of DNA-dependent ATPases involved in chromatin remodeling. Like the rad26 mutant, cells from Cockayne syndrome patients are defective in TCR. We examined the role of Rad26 in TCR by disrupting RAD26 in two repair-proficient laboratory strains and, remarkably, observed no effect upon TCR. Our results indicate that disruption of RAD26 alone is insufficient to impair TCR. Thus, W303-1B must already possess a mutation that, together with disruption of RAD26, causes a deficiency in TCR. We suggest that other genes are mutated in Cockayne syndrome cells that contribute to the deficiency in TCR. Surprisingly, deletion of RAD26 results in expression of genes that are repressed by flanking transposon 
elements, an Spt– phenotype. The elements appear to perturb local chromatin structure. Expression of genes flanked by elements in rad26
mutants is consistent with a role for Rad26 in chromatin remodeling.
* To whom correspondence should be addressed. Tel: +1 732 445 3400; Fax: +1 732 445 0687; Email: sweder{at}rci.rutgers.edu
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