## 4 Discussion
### Function of Genes Co-Regulated with the UV-B-Marker CHS  
Two TF genes, _MYB23_ and _ERF38_, were identified (Figure S4A), and MYB23 is involved in trichome initiation which is positively regulated by UV-B. In addition to their repelling function towards insects, trichomes are also thought to protect the shaded tissue from UV-B radiation [46; 47]. ERF38 is considered a candidate regulator of secondary wall metabolism in cell types that are not reinforced by the typical deposition of lignin but display suberization [48]. While ERF38 has not been linked to trichome development, several other TFs identified in Table 2A are involved in this process (GTL1, MYC1, and the WD40 protein FAS2).  
MYB111 was distantly linked to SPCH, MYC1, and HB31 (Figure S4B). The positive regulator MYB111 has already been linked to this crosstalk as capable to activate _CHS_ expression [6; 19]. SPCH and MYC1 are both bHLH TFs, with SPCH being involved in stomatal development and indirectly stabilized by HY5-mediated expression of STOMA  
Figure 3: Graphical summary of potentially new processes involved in crosstalk between pathogen and UV-B induced signaling as discussed in the text. Identification of several conversely regulated MYB, bHLH, and WD40 TFs (Table 1) suggests that MBW complexes consisting of these TFs might also be regulating the “early” FPGs. Positive influence on FPG expression is deduced from genes that are co-regulated together with the _CHS_ marker gene (being UV-B up- and flg22 down-regulated), while the negative impact is assumed from genes that are co-regulated with the _FRK1_ marker gene (being UV-B down- and flg22 up-regulated).  
GEN [49; 50]. Its suppression during PTI might be of advantage when reducing potential entry points of pathogens, but there is no link to UV-B-related responses so far.  
Figure S4C links bZIP61, bZIP34, GTL1 and HAT1. Both bZIP61 and bZIP34 have been found to form heterodimers with bZIP18 and bZIP52 [51] and bind to the G-Box [52], but all these TFs have not been reported in the regulation of FPG expression before. GTL1, a trihelix TF, acts to interfere with trichome cell differentiation [53] and the trichome branch length [54]. HAT1 might function in a negative feedback mechanism, e.g., via interaction with MYB75, thereby interfering with MBW protein complex formation to stop the expression of the FPGAs [55].  
We found several interesting candidates, including UNE10, a bHLH TF, and the three Arabidopsis Whirly TFs, which cluster together with MYB29 and MYB75 (Figure S3A). Both MYB29, as well as UNE10, are negative regulators and the latter can inhibit Phytochrome A-mediated far-red light responses [56]. UNE10 is one of three TFs that were stronger induced by UV-B, with an additional attenuating effect on flg22-mediated suppression observed in the co-treatment (Table 2A, together with MYB111 and SPCH). Co-regulation of CHs with the Whirly TFs constitutes another link to chloroplast and mitochondrial retrograde signaling. WHY1 is targeted to the chloroplast, while WHY2 is targeted to the mitochondria [57]. Interestingly, [PERSON] et al. [58] showed that anthocyanin levels are strongly suppressed in the _why1/why3/pollb_ triple mutant. The suppression of WHY1, WHY2, and WHY3 during elicitor-induced PTI can be deduced (Figure S2). In the _why1_ mutant, H\({}_{2}\)O\({}_{2}\) and SA were induced earlier during senescence development [59; 60], and immunity-related genes such as PR-1 were activated [61]. Thus, the suppression of Whirly TFs found in this study might be important for the integrity of flg22-induced plant immunity.