Figure 7
From: Nitric oxide participates in plant flowering repression by ascorbate
Flowering time change of A. thaliana Col-0 (Wt), and noa1 mutant in response to exogenous L-galactonolactone (L-GalL) treatment.
(a) The effect of L-galactonolactone (L-GalL) on the flowering time of A. thaliana Col-0 (Wt) and noa1 (scale bar = 1cm). (b) The percentage of flowering Wt or noa1 at different development stages specified according to rosette leaf number under mock or L-GalL treatments (n wt and nnoa1 ≥30). Error bars indicate standard deviation (s.d.). Asterisks represent significant differences between samples as determined using two-way ANOVA (Wt; *p < 0.05; **p < 0.005; ***p < 0.0005). (c) The ascorbic content and ratio of reduced/oxidized form of AsA in A. thaliana Col-0 (Wt) and noa1 grown in ½ MS without treatment (mock: (
), Wt; (
), noal mutant), or under treatment with 20 μM SNP (
), Wt; (
), noa1 mutant) for 3 weeks. Significant differences compared with mock were analyzed by two-way ANOVA (*p < 0.05; **p < 0.005; ***p < 0.0005). (d) Working model of the Oncidium floral repression acquired by post-translational modification of NO- biosynthesis-related enzymes: During the vegetative stage, the AsA level, NO-related enzymes (NaR, NiR and NOS) and NO levels were high and synergistically repressed flowering. In the bolting stage, DHA was produced by the redox homeostasis of Oncidium, which lowered the AsA redox ratio, thus leading to deceased NO-related enzymatic activities for NO and phase transition. In the next vegetative stage, low levels of AsA and NO were triggered by the redox homeostasis, thus leading to the accumulation of GSNO to terminate the reproductive stage through floral repression and post-translational modification of APX.
