Biology Reference
In-Depth Information
GA Application Fails to Induce the Expression of MYB21,
MYB24 and MYB57 in JA-Deficient Mutant
We showed in the above that the expression of MYB21, MYB24 and MYB57
was repressed in the ga1-3 gai-t6 rga-t2 rgl1-1 quadruple mutant (wild type for
RGL2) but restored to normal in the ga1-3 gai-t6 rga-t2 rgl1-1 rgl2-1 penta
mutant (Figure 2A and 2B). Mandaokar et al reported that the expression of
MYB21 and MYB24 was downregulated in opr3 mutant and application of ex-
ogenous JA could restore their expression [32]. These results suggest that there
might be a crosstalk between the GA and JA pathways in regulating the expres-
sion of MYB21, MYB24 and MYB57 during stamen development. Genetically,
there are three possible ways of interaction between GA and JA. Firstly, GA
might act through the JA pathway to regulate the expression of these MYB genes.
In this case it is expected that JA application onto ga1-3 gai-t6 rga-t2 rgl1-1
would induce the expression of MYB21, MYB24 and MYB57 whilst GA ap-
plication onto opr3 would have no effect on their expression. Conversely, JA
may act upstream of the GA pathway to regulate the expression of these three
MYB genes. In this case, GA application onto opr3 would induce whilst JA ap-
plication onto ga1-3 gai-t6 rga-t2 rgl1-1 would have no effect on the expression
of MYB21, MYB24 and MYB57. The third possibility is that GA and JA may
not act in a hierarchical manner but rather via parallel pathways to regulate the
expression of the three MYB genes. If this is the case, GA application onto opr3
and JA application onto ga1-3 gai-t6 rga-t2 rgl1-1 would probably both induce
the expression of the three MYB genes. To find out which is the likely case, we
first examined the effect of GA application on JA-deficient mutant opr3 and
found that GA application failed to rescue the opr3 mutant phenotype and failed
to induce the expression of MYB21, MYB24 and MYB57 in opr3 even at 96 hrs
after GA treatment (Figure 5A). Failure in induction of expression of MYB21,
MYB24 and MYB57 in GA-treated opr3 mutants could be due to inactivation
of GA signaling in JA-deficient background. GA3ox1 and GA20ox2 are two key
genes that contribute to the biosynthesis of bioactive GA and these two genes are
under negative feedback regulation by GA signaling pathway (GA-down) [30].
On the other hand, GA2ox1 is a GA-up gene responsible for GA catabolism
[30]. Examination of the GA3ox1 and GA20ox2 and GA2ox1 expression in GA-
treated opr3 mutants showed expected GA-response (Figure 5B). Meanwhile,
expression of GA3ox1 and GA2ox1 appeared normal in opr3 (Figure 6A). These
results suggest that JA-deficiency specifically blocks the GA-signaling leading to
the induction of MYB21, MYB24 and MYB57 expression but not the negative
feedback pathway for GA-biosynthesis.
