The interplay of transcription factors in suppression of UV-B induced flavonol accumulation by flg22

Abstract

Biotic stress can be mimicked by application of elicitors, which comprise of microbe-associated molecular patterns (MAMPs). Treatment of plant cell cultures with MAMPs such as flg22 suppressed the expression of UV-B-induced flavonol pathway genes (FPGs) in parsley, carrot and Arabidopsis. This is thought to allow the plant focusing its secondary metabolism on the pathogen defense during MAMP-triggered immunity (MTI). Recently we reported that this suppression also depends on prevention of histone 3 acetylation at lysine 9 (H3K9ac), a hallmark for gene activation. Here we describe a possible regulation between UV-B and flg22 signaling cascades, and the interplay of MYB and WRKY transcription factors in regulating the expression of the FPGs.

Keywords: ChIP; H3K9ac; HY5; MYB; UV-B; WRKY; crosstalk; flg22; histone modification.

Figure 1. Working model displaying the interaction of transcription factors in regulation of the flavonol pathway genes (FPGs). The suppressive effect of flg22-induced signaling (MTI) on UV-B-activated FPG expression may be mediated by WRKY TFs via downregulating the positive regulator MYB12 and/or upregulating the negative regulator MYB4. The two MYB TFs are good candidates to recruit HAT or HDAC activity, respectively, thereby being responsible for changes in H3K9 acetylation at the FPG loci.

Figure 2. In silico promoter analysis of the negative regulator MYB4 and the positive regulator MYB12. The arrows within the boxes, which represent cis responsive elements, indicate the orientation (forward or reverse complement).