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. 2015 Nov 27;472(Pt 3):379–391. doi: 10.1042/BJ20150147

Figure 5. Inhibition of phosphorylation of specific activation segment residues through site-directed mutagenesis differentially impairs growth signalling by PSKR1 in seedling roots.

Figure 5

(A) Seedlings of up to five independent transgenic lines of the PSKR1(T890A), PSKR1(S893A/T894A), PSKR1(T899A), and PSKR1(TSTT-A) mutants in the receptor-null r1r2 background were grown with or without 1 μM PSK for 5 days. Mean±S.E.M. root lengths were determined in three independent experiments with at least 48 seedlings analysed per genotype. Asterisks indicate significantly different values between r1r2 and the lines expressing different receptor variants (P<0.001, two-sample Student's t test). Circles indicate significantly different values between treatments for each genotype (n≥32; P<0.001). (B) Mean±S.E.M. root lengths were determined in five independent lines of the phosphomimic receptor variant PSKR1(T890D) expressed in the receptor-null r1r2 background. At least 57 seedlings were analysed per genotype in three independent experiments in the absence or presence of 1 μM PSK. Asterisks indicate significantly different values between r1r2 and the PSKR1(T890D) lines (P<0.001, two-sample Student's t test). Circles indicate significantly different values between treatments for each PSKR1(T890D) line (n≥50; P<0.001). S/T893/4A, S894A/T894A; wt, wild-type.