Transcription coupled repair (TCR) is a nucleotide excision repair (NER) pathway 
that is dedicated to repair in the transcribed strand of an active gene. The 
genome overall NER is called global genomic repair (GGR). Elc1, the yeast 
homolog of the mammalian elongation factor elongin C, has been shown to be a 
component of a ubiquitin ligase complex that contains Rad7 and Rad16, two 
factors that are specifically required for GGR. Elc1 has also been suggested to 
be present in another ubiquitin ligase complex that lacks Rad7 and Rad16 and is 
involved in UV-induced ubiquitylation and subsequent degradation of RNA 
polymerase II. Here we show that elc1 deletion increases UV sensitivity of 
TCR-deficient cells but does not affect the UV sensitivity of otherwise wild 
type and GGR-deficient cells. Cells deleted for elc1 show normal NER in the 
transcribed strand of an active gene but have no detectable NER in the 
non-transcribed strand. Elc1 does not affect UV-induced mutagenesis when TCR is 
operative, but plays an important role in preventing the mutagenesis if TCR is 
defective. Furthermore, the levels of Rad7 and Rad16 proteins are not 
significantly decreased in elc1 cells, and overexpression of Rad7 and Rad16 
individually or simultaneously in elc1 cells does not restore repair in the 
non-transcribed strand of an active gene. Our results suggest that Elc1 has no 
function in TCR but plays an important role in GGR. Furthermore, the role of 
Elc1 in GGR may not be subsidiary to that of Rad7 and Rad16.