Extended Data Fig. 4: SnRK1β1A is up-regulated upon infection by rice major fungal pathogens and negatively regulates rice immunity.
From: Inactivating SnRK1β1A promotes broad-spectrum disease resistance in rice
a–f, Expression levels of SnRK1β1A in NPB after infection by M. oryzae (a), F. graminearum (b), F. fujikuroi (c), B. oryzae (d) R. solani (e) and U. virens (f) at the indicated time points. H2O treatment served as a control. g, Schematic representation of the SnRK1β1A gene structure and gene editing sites. Bold letters indicate PAM, “-” indicates nucleotide deletion, and red letter indicates nucleotide insertion. h, Infection assay showing that snrk1β1a mutants are resistant to diverse isolates of M. oryzae, including SZ-4 and SZ-2. Fungal biomass was measured by qPCR at 5 dpi. i, The leaf sheath cells of snrk1β1a lines showed a higher frequency of ROS production than those of WT ZH11 after infection by M. oryzae strain SZ-5. At 36 hpi, rice leaf sheath cells were stained with DAB, and the percentage of infected sites with DAB-stained cells was calculated. Scale bars, 20 μm. j, Higher levels of ROS production were induced in snrk1β1a lines than in WT ZH11 upon chitin treatment. Rice leaf discs were immersed in 0.5 μM chitin to detect ROS using the Luminol assay. k,l, snrk1β1a lines showed stronger MAPK activation and PR gene induction upon chitin treatment than WT ZH11. One-week-old rice seedlings were treated with 0.5 μM chitin for 0–60 min and collected for phosphorylated MAPK detection using an anti-phospho-p44/42 antibody, with anti-Actin as a loading control, and for measuring the expression of PR genes by RT-qPCR after 6 h. Data represent mean ±s.d.; n = biologically independent samples in the graphs. Two-tailed Student’s t tests were employed in (h,l), **P < 0.01. For exact P values, see Source Data. All experiments were repeated at least three times with similar results. RLU, relative luminescence units.
