"However, we found that loss-of-function mutations in the gene
haf-1, which encodes a mitochondrial outer membrane ABC transporter previously shown to function as an activator of the mitochondrial unfolded protein response (mitoUPR), significantly suppressed the hypoxia resistance of both ub-m-nonN-Nmnat1 and neuro-m-nonN-Nmnat1 transgenes (Figures 3a and b)."