Both -dependent and independent pathways are involved in DNA damage-associated sister chromatid exchange in budding yeast.

Sister chromatids are preferred substrates for recombinational repair after cells are exposed to DNA damage. While some agents directly cause double-strand breaks (DSBs), others form DNA base adducts which stall or impede the DNA replication fork. We asked which types of DNA damage can stimulate SCE in budding yeast mutants defective in template switch mechanisms and whether PCNA polyubiquitination functions are required for DNA damage-associated SCE after exposure to potent recombinagens. We measured spontaneous and DNA damage-associated unequal sister chromatid exchange (uSCE) in yeast strains containing two fragments of after exposure to MMS, 4-NQO, UV, X rays, and HO endonuclease-induced DSBs. We determined whether other genes in the pathway for template switching, including , , , and were required for DNA damage-associated SCE. was required for DNA damage-associated SCE after exposure to UV, MMS, and 4-NQO, but not for spontaneous, X-ray-associated, or HO endonuclease-induced SCE. While , , and were required for MMS and 4NQO-associated SCE, they were not required for UV-associated SCE. DNA damage-associated recombination between recombination substrates on non-homologous recombination was enhanced in mutants. These results demonstrate that DNA damaging agents that cause DSBs stimulate SCE by -independent mechanisms, while several potent agents that generate bulky DNA adducts stimulate SCE by multiple -dependent mechanisms. We suggest that DSB-associated recombination that occurs in G2 is -independent.