Rev1 deficiency induces a metabolic shift in MEFs that can be manipulated by the NAD+ precursor nicotinamide riboside

Replication stress, caused by Rev1 deficiency, is associated with mitochondrial dysfunction, and metabolic stress. However, the overall alterations possible interventions to rescue deficits due loss remain unclear. Here, we report that of leads intense changes in metabolites this can be manipulated NAD + supplementation. Autophagy decreases Rev1−/− mouse embryonic fibroblasts (MEFs) restored supplementing NAD+ precursor nicotinamide riboside (NR). The abnormal morphology MEFs partially reversed NR supplementation, which also protects cristae from rotenone-induced degeneration. In nematodes rev-1 deficiency causes sensitivity oxidative stress but cannot rescued conclusion, dysregulation especially lipid nucleotide metabolism, impaired autophagy, anomalies, all these phenotypes improved replenishment MEFs.