Fig. 4. R236 methylation of PHGDH mediated by PRMT1 promotes serine synthesis and ameliorates oxidative stress.

a–e PHGDH was knocked out (PHGDH KO) using CRIPSR/Cas9 technology, followed by re-expression of PHGDH WT, R236K (RK) or V83A (VA). Immunoblotting was performed with indicated antibodies (a). Incorporation of U-[¹³C]-glucose carbon into serine (b) and glycine (c) was detected by LC-MS/MS. GSH (d) and ROS (e) levels were measured in these cells grown in CM or -SG medium. Data in b–e are presented as the mean ± SD (n  =  3 independent experiments). Statistical analysis was performed using the two-tailed Student’s t-test. f–j PHGDH KO plus PRMT1 KD cells were rescued with PHGDH WT, R236K (RK) or V83A (VA), combining with or without PRMT1 re-expression. Immunoblotting was performed with indicated antibodies (f). Incorporation of U-[¹³C]-glucose carbon into serine (g) and glycine (h) was detected by LC-MS/MS. GSH (i) and ROS (j) levels were measured in cells grown in CM or -SG medium. Data in g–j are presented as the mean ± SD (n  =  3 independent experiments). Statistical analysis was performed using the two-tailed Student’s t test. Source data are provided as a Source Data file.