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Legend Who Seems To Be Fearful Of Panobinostat

We chose the DFR, Selleckchem Bortezomib F3H and FLS1 mutants tt3-1, tt6-1 and fls1-1, respectively, because they represent key branch points in the pathway (Figure?1a and Figure S4), allowing us to group the possible effects of flavonoids into four types, i.e. those of naringenin itself (I), flavonols (II), an intermediate in the pathway downstream of naringenin but not a flavonol (III), and a compound downstream of DFR, most likely an anthocyanin (IV). The quantitative RT-PCR analyses of the seven genes in the tt3-1, tt6-1 and fls1-1 mutants provided interesting but unexpected patterns (Figure?3). The induction of four of the seven naringenin-induced genes (PDR12, NAR1, PER41 and the MATE gene) was significantly reduced in tt3 (Figure?3). This suggests that a product downstream of DFR is responsible for induction of these genes, or that a pathway intermediate that accumulates in tt3, but not in WT, inhibits their induction by naringenin. If a product downstream of DFR were responsible for the induction, then the induction would also be significantly blocked in the tt6 mutant. This was not the case for any of the four genes (Figure?3), suggesting that perhaps a product upstream of DFR has an inhibitory effect. Among others, such Panobinostat inhibitory compounds may be dihydroflavonols or flavonols (Figure?1a). If the inhibitory compounds were dihydroflavonols, a similar reduction would be observed in the fls1 mutant, which was not the case for any of the genes (Figure?3). If the inhibitory compounds were flavonols, naringenin would induce expression in fls1, which is what we observed for PER41 (P?<?0.05) and the MATE gene (P?<?0.01), with a similar pattern but less statistical support for NAR1 and PDR12 (Figure?3). These results suggest that one or more flavonol compounds play a repressive role in steady-state mRNA accumulation for PDR12, NAR1, PER41 and the MATE gene. Moreover, the ability of naringenin to induce PDR12, NAR1 <a href="">MAPK inhibitor and NRT3.1 expression in tt5 suggests that a compound downstream of TT3/DFR that is specifically present in tt5 (perhaps a chalcone) has an activating role on expression of these genes. Naringenin appears to be the inducer for PSK4 and, to a lesser extent, for GST21 (Figure?3). In fact, both genes are significantly induced in tt6 after naringenin treatment (P?<?0.01). PSK4 is robustly and very significantly (P?<?0.01) induced by naringenin in all the mutants tested (Figure?3). To further investigate the regulation of the PSK4 gene, we measured its promoter activity after induction with naringenin. We used transgenic plants containing the PSK4 promoter fused to the uidA reporter gene encoding ��-glucuronidase (GUS) (Matsubayashi et?al., 2006). Five-day-old ProPSK4:uidA seedlings were grown on AIC with or without Nar. GUS activity (see Methods S1) was increased in seedlings induced by naringenin, supporting the finding that the PSK4 promoter is induced in the presence of naringenin (Figure?4).</div>
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