Fig. 3: Pi starvation–induced m6A modifications are largely mediated by PHRs.

a, b m6A-seq clustering (a) and principal component analysis (PCA) (b) confirming the high reproducibility between biological replicates and the differences between the WT and phr1 phl1 samples under −P but not +P conditions. c Box plots showing a significant decrease in m6A modification levels in phr1 phl1 compared with the WT under −P but not +P conditions. +P WT, n = 11,472; +P phr1phl1, n = 11,923; −P WT, n = 12,513; −P phr1phl1, n = 12,378. d Volcano plot of m6A enrichment, with 3265 hypomethylated m6A peaks and 477 hypermethylated m6A peaks in phr1 phl1 compared with the WT under −P conditions. FDR value was calculated using a one-tailed rescaled hypergeometric test. e, f Venn diagrams showing PHR-mediated PSI-m6A peaks (P = 0) (e) and PHR-mediated PSD-m6A peaks (P = 1.90e-49) (f). **P < 0.01, the one-tailed hypergeometric test. g Violin plots showing a significant decrease in m6A modifications of PHR-mediated PSI-m6A genes (n = 1931) in phr1 phl1 compared with the WT under −P but not +P conditions. h IGV view of the m6A-seq signals of selected PHR-mediated PSI-m6A genes. In (c and g), P values were calculated using the two-tailed Wilcoxon test. The midlines and box edges indicate the medians and quartiles, respectively. The whiskers extend to the farthest data point within 1.5 times the interquartile range (IQR) from the box edges.