Fig. 1: NPEs promote desensitisation of ABA transcriptional response.
From: N-glycosylation of SnRK2s affects NADPH maintenance in peroxisomes during prolonged ABA signalling
a, c, e The morphological analyses showed that NPEs negatively regulate ABA signalling. Arabidopsis plants were seeded and grown on 1/2 × MS medium either lacking or supplemented with 3 μM ABA. Photographs of representative seedlings were taken after 10 d ABA treatment for (a) and (c), and 12 d for (e). Col-0 seedlings were used as a control. Scale bars, 1 cm. a ABA-treated gIIβ−2 and two complementation lines (com-1 and com-2), n = 3 plants. c ABA-treated stt3a-2 and STT3A-OE line 13, n = 3 plants. e ABA-treated rsw3, fuc11, cgl1-T, and hgl1-2, n = 6 plants. b, d, f The relative primary root length is shown in (a), (c), and (e), respectively. The relative root length was calculated as the ratio of ABA-treated roots by no ABA-treated roots (ABA + /−), and it was designated as 1 in Col-0. Data are means ± s.d. Asterisks indicate significant differences (*P-value < 0.05, ** P-value < 0.01, ***P-value < 0.001), as determined by two-tailed paired t tests. “ns” means no significant difference. g–i Desensitisation of the transcription of ABA-responsive genes NCED3, P5CS1 and RAB18 is positively regulated by STT3A. Data are means ± SEM. from 3 biological replicates. j, k STT3A genome-widely controls desensitisation of ABA transcriptional response. j The temporal expression pattern of 1288 ABA-induced genes in cluster 1 in ABA-treated Col-0. 2.3% of total genes whose associated GO terms respond to abiotic stress. k Comparative expression analyses of 1288 ABA-induced genes in Col-0 without ABA treatment (CK), Col-0 and stt3a-2 treated with 50 μM ABA. The red arrowheads denote the expression inflection point from activation to desensitisation during prolonged ABA signalling in fig. g–i and fig. k.
