Together this suggests that a prototypical FA-related ICL repair pathway operates in budding yeast, which acts redundantly with the pathway controlled by Pso2, and is required for the targeting of Exo1 to chromatin to execute ICL repair.
To evaluate the epistatic relationship between hSNM1 and other ICL repair pathways, we depleted hSNM1 in Fanconi anemia (FA) cells, which are inherently sensitive to ICLs.
The homology of the KIAA0086 gene to the yeast SNM1 gene, which is involved in the cellular response to DNA-interstrand crosslinks, is discussed with respect to a possible role of the KIAA0086 gene in the human disorder, Fanconi anemia.