In both yeast and humans, DNA polymerase (Pol) eta functions in error-free
replication of ultraviolet-damaged DNA, and Pol eta promotes replication th
rough many other DNA lesions as well. Here, we present evidence for the phy
sical and functional interaction of yeast Pol eta with proliferating cell n
uclear antigen (PCNA) and show that the interaction with PCNA is essential
for the in vivo function of Pol eta. Pol eta is highly inefficient at inser
ting a nucleotide opposite an abasic site, but interaction with PCNA greatl
y stimulates its ability for nucleotide incorporation opposite this lesion.
Thus, in addition to having a pivotal role in the targeting of Pol eta to
the replication machinery stalled at DNA lesions, interaction with PCNA wou
ld promote the bypass of certain DNA lesions.