Abasic or AP sites generated by spontaneous DNA damage accumulate at a higher 
rate in actively transcribed regions of the genome in S. cerevisiae and are 
primarily repaired by base excision repair (BER) pathway. We have demonstrated 
that transcription-coupled nucleotide excision repair (NER) pathway can 
functionally replace BER to repair those AP sites located on the transcribed 
strand much like the strand specific repair of UV-induced pyrimidine dimers. 
Previous reports indicate that Rad26, a yeast homolog of transcription-repair 
coupling factor CSB, partly mediates strand-specific repair of UV-dimers as well 
as AP lesions. Here, we report that Def1, known to promote ubiquitination and 
degradation of stalled RNA polymerase complex, also directs NER to AP lesions on 
the transcribed strand of an actively transcribed gene but that its function is 
dependent on metabolic state of the yeast cells. We additionally show that Dst1, 
a homolog of mammalian transcription elongation factor TFIIS, interferes with 
NER-dependent repair of AP lesions while suppressing homologous recombination 
pathway. Overall, Def1 and Dst1 mediate very different outcomes in response to 
AP-induced transcription arrest.