Deletion mutants of CHL1 or CTF4, which are required for sister chromatid 
cohesion, showed higher sensitivity to the DNA damaging agents methyl 
methanesulfonate (MMS), hydroxyurea (HU), phleomycin, and camptothecin, similar 
to the phenotype of mutants of RAD52, which is essential for recombination 
repair. The levels of Chl1 and Ctf4 associated with chromatin increased 
considerably after exposure of the cells to MMS and phleomycin. Although the 
activation of DNA damage checkpoint did not affected in chl1 and ctf4 mutants, 
the repair of damaged chromosome was inefficient, suggesting that Chl1 and Ctf4 
act in DNA repair. In addition, MMS-induced sister chromatid recombination in 
haploid cells, and, more importantly, MMS-induced recombination between 
homologous chromosomes in diploid cells were impaired in these mutants. Our 
results suggest that Chl1 and Ctf4 are directly involved in homologous 
recombination repair rather than acting indirectly via the establishment of 
sister chromatid cohesion.