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 delta elements, an Spt(-) phenotype. The delta elements appear to 
perturb local chromatin structure. Expression of genes flanked by delta elements 
in rad26Delta mutants is consistent with a role for Rad26 in chromatin 
remodeling.