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Figure 5.
JA-Deficiency Specifically Blocks GA-Signaling Leading to the Induction of Expression of MYB21,
MYB24, and MYB57.
(A-B) Semi-quantitative
analysis of MYB21, MYB24, MYB57 (A), GA2ox1, GA3ox1 and GA20ox2 (B)
expression in the opr3 mutant flowers at 18, 48, 72 and 96 hrs after GA treatment. Data were averaged from
2-4 batches of independently treated samples and ACTII was used as the normalization control. The graph was
drawn based on Log10 scale of the ratio of the expression levels of GA treated versus untreated samples. (C-D)
Semi-quantitative analysis of LOX2 (in red line), GA2ox1, GA3ox1 and GA20ox2 (C), MYB21, MYB24 and
MYB57 (D) expression in the ga1-3 gai-t6 rga-t2 rgl1-1 (Q3) mutant flowers at 18, 48, 72 and 96 hrs after JA
treatment. Data were averaged from 2-4 batches of independently treated samples and ACTII was used as the
normalization control. The graph was drawn based on Log10 scale of the ratio of the expression levels of JA
treated versus untreated samples.
JA Application Restores the Expression of MYB21, MYB24
and MYB57 in GA-Deficient Mutant
We then studied the effect of JA application on ga1-3 gai-t6 rga-t2 rgl1-1 (GA-
deficient) by examining the expression of MYB21, MYB24 and MYB57 in the
young flower buds at 18, 48, 72 and 96 hrs post-treatment. As expected, LOX2,
a JA-response gene, was strongly upregulated by JA application at 18 hrs post
treatment (Figure 5C) [39]. Interestingly, we observed that JA-treatment induced
high expression of MYB21 and MYB24 and weak expression of MYB57 in the
ga1-3 gai-t6 rga-t2 rgl1-1 quadruple mutant at 18 hrs post treatment (Figure
5D). However, examination of GA3ox1 and GA20ox2 (two GA-down genes)
