Fig 1: Coordinated regulation of ribosome and proteasome component proteins during neuronal differentiation.A and B, RA-induced neuronal differentiation phenotype in NE-4C cells shown at the time indicated after treatment (A), and immunoblotting (IB) detection of a series of proteasome, ribosome components, epigenetic factors, and neural stemness and neuronal proteins in control cells treated with vehicle (DMSO) and cells treated with RA, as indicated (B). C and D, neuronal differentiation phenotype in NE-4C cells induced by Prmt1 knockdown at the indicated time (C), and IB detection of expression of proteins, as indicated, in control (shCtrl) and knockdown (shPrmt1) cells (D). E, IB detection of various proteins, as indicated, in control A549 (shCtrl) cells and cells with knockdown of PRMT1 (shPRMT1). F, IB detection of various proteins, as indicated, in mouse embryonic cortical cells at two developmental stages. G, IF detection of the effect of PRMT1 knockdown on the subcellular distribution of ribosome components RPS3 and RPL26, proteasome protein PSMD2 and 20S subunit (20S a + ß) in A375 cells. H, IF detection of the effect of PRMT1 overexpression on the expression of ribosome and proteasome proteins in A549 cells. Cells infected with the virus containing only the vector (Vector) as a control. I, detection of the change in 5S and 5.8S rRNA in A549 cells with PRMT1 knockdown or overexpression using RT-qPCR. Significance in change of rRNA levels was calculated for experiments in triplicate using unpaired Student’s t test. Data are shown as mean ± SD. ***p < 0.001, ****p < 0.0001.