Roles of JA in regulating catechin biosynthesis under HT
It has been demonstrated that JA plays an important role in the
regulation of flavonoid biosynthesis, including proanthocyanidins and
anthocyanins (An et al., 2015). When tea plants were exposed to HT, we
noticed that JA-responsive genes including CsLOX1 , CsAOS ,
and CsMYC2 were down-regulated, suggesting impaired JA signaling
to be associated with HT exposure (Figure 3a). Given the lower content
of MeJA in HT-treated tea leaves (Figure 3b), we wondered whether the JA
pathway mediates the inhibiting effect of HT on catechin biosynthesis.
After spraying tea leaves with MeJA, ibuprofen (a JA synthesis
inhibitor), and MeJA plus MG132, we then transferred pre-treated plants
into growth chambers to grow at 25 ℃ or 40 ℃ for 3 d. Subsequent HPLC
analysis revealed that HT significantly reduced catechin content with an
average reduction of 15.5%, and ibuprofen treatment also repressed
catechin accumulation by 32.8%, whereas treatment with MeJA alleviated
the inhibitory effect of HT on catechin biosynthesis, resulting in
catechin levels about equal to those in plants grown at normal
temperature (Figure 3c). Consistent with the observed changes in
catechin levels, expression of biosynthetic genes includingCsCHS , CsDFR , and CsANS was significantly inhibited
in plants sprayed with ibuprofen and the expression patterns resembled
those in plants treated with HT, whereas MeJA was able to partly
counteract the inhibition caused by HT (Figure 3d).