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In this report, we first identified 34 DELLA-repressed stamen-enriched genes
by RT-PCR analysis of candidate genes selected from microarray data [30]. We
then selected MYB21, MYB24 and MYB57 for detailed genetic analysis because
GAMYBs are the best characterized transcription factors involved in GA-response.
We showed that Arabidopsis MYB21, MYB24 and MYB57 are highly expressed
in the stamen. The stamen-enriched expression pattern is consistent with the ob-
servation that the myb21-t1 myb24-t1 myb57-t1 triple mutant is impaired in the
stamen development, especially in the stamen filament elongation. During the
course of studying these three MYBs, Mandaokar et al reported that MYB21 and
MYB24 are also JA-inducible [32] which immediately attracted our attention to
study the hierarchical relationship between GA and JA in regulating the expres-
sion of these three MYBs.
We first tested the responses of GA- and JA-deficient mutants (i.e. ga1-3 gai-
t6 rga-t2 rgl1-1 Q3 quadruple mutant and opr3 mutant, respectively) to GA and
JA treatments and found that JA- treatment induced the expression of MYB21,
MYB24 and MYB57 in the GA-deficient plants whereas GA-treatment failed to
do so in the JA-deficient plant. This result suggests that JA likely acts downstream
of GA pathway to control the expression of these three MYBs. It is possible that
JA acts downstream by modulating the stability or activity of DELLA proteins to
induce the expression of the three MYBs. If this is the case, we would expect that
JA-treatment would lead to RGL2 degradation or would change the expression
patterns of GA-response genes in ga1-3 gai-t6 rga-t2 rgl1-1. However, we found
that neither the RGL2 protein level (data not shown) nor the expression patterns
of three GA-response genes GA2ox1, GA3ox1 and GA20ox1 were obviously
altered in the JA-treated ga1-3 gai-t6 rga-t2 rgl1-1 plants at 18 hrs post treat-
ment although the three MYBs are highly expressed at this time point, suggesting
that destabilization or inactivation of DELLA proteins is unlikely the cause for
JA-induced expression of MYBs in ga1-3 gai-t6 rga-t2 rgl1-1. Alternatively, it is
possible that GA suppresses DELLA to promote JA production or modulate JA-
signaling to induce the expression of the three MYBs. The fact that JA application
can restore the expression of the three MYBs in the GA-deficient background
strongly suggests that, at least in part, JA biosynthesis is impaired in the ga1-3
gai-t6 rga-t2 rgl1-1 mutant.
JA biosynthesis is accomplished by a sequential biochemical reactions medi-
ated by JA-biosynthesis genes including DAD1, LOX1, 2, AOS, AOC1, 2, 3, 4
and OPR3 and is regulated by OPDA compartmentalization and a JA-mediated
positive feedback loop [41]. Biotic and abiotic stresses also induce JA forma-
tion [42]-[44]. In our experiment, we found that JA biosynthesis gene DAD1
was greatly down-regulated in both ga1-3 single and ga1-3 gai-t6 rga-t2 rgl1-1
