## 3 Results
### RNAseq Data Support Our Previously Postulated Working Model  
Based on a KEGG enrichment analysis of DEGs from CHS-group and FRK1-group, there are several indications that the phenylpropanol pathway (ath00940), including  
Figure 1: Impact of crosstalk on transcriptomic changes in Arabidopsis. (**A**) An overview of DEGs identified from RNAseq experiments using pooled RNA of three independent biological replicates. Treatments with fig22 (F), UV-B (U), or co-treatment with fig22 and UV-B (F/U) as compared to the control. DEGs were identified by applying a log2 threshold \(\leq-1\) or \(\geq 1\) for each treatment. Since we detected approximately five-fold fewer DEGs in the UV-B samples we lowered the log2 threshold to \(\pm 0.2\) for this treatment in order to obtain a comparable number of DEGs as in the other treatments. (**B**) A Venn diagram displaying the number and distribution of DEGs that were down-regulated in response to single and co-treatment fig22, but up-regulated by UV-B (CHS-group). (**C**) A Venn diagram displaying the number and distribution of DEGs that were up-regulated in response to single and co-treatment with fig22, but down-regulated by UV-B (FRK1-group). The DEG numbers shown in (**B**,**C**) are based on a log2 threshold \(\leq-1\) or \(\geq\)1 for fig22 or F/U co-treatment with the log2 threshold for the UV-B treatment lowered to \(\pm 0.2\). (**D**) Cluster analysis of genes involved in phenylpropanol metabolism shows the expected expression patterns with genes involved in the flavonoid pathway (FPG and anthocyanin biosynthesis-related genes) being largely up-regulated by UV-B and suppressed in response to fig22 and containing the _CHS_ marker gene (Cluster I) as well as genes being up-regulated in response to fig22 (Cluster II), belonging to the general phenylpropanol (GPP), monolignol (MPG), lignin (LPG) or coumarin (CPG) pathways clustering together with the _FRK1_ marker gene for successful induction of pattern triggered immunity (PTI). Expression levels are calculated based on log2-fold changes relative to the untreated control. Gene name abbreviations and concrete log2 values underlying the calculation can be found in Table S3. flavonoid biosynthesis (ath00941) and anthocyanin biosynthesis (ath00942), displays major changes in this crosstalk (Table S4). Therefore, the hierarchical clustering of the relative gene expression (log2-fold change) of 45 DEGs encoding structural genes of the phenylpropanol pathway was investigated in the context of this crosstalk. Generally, genes in Cluster I are suppressed by F or the co-treatment F/U and mostly up-regulated by UV-B (such as the marker gene _CHS_), while Cluster II genes are up-regulated by F or F/U, but negatively affected by UV-B treatment (such as the _FRK1_ marker gene). The result is consistent with previous qPCR data from Arabidopsis cell cultures and Arabidopsis meta-data [5] (Figure 1D and Table S3), demonstrating that flavonoid biosynthesis pathway genes (FPGs) are generally suppressed by single F or F/U co-treatment in Arabidopsis plants. In addition, anthocyanin biosynthetic-related genes _LDOX/ANS_ and _DFR_ showed a similar expression pattern as the FPGAs. Here, the crosstalk marker gene _CHS_ displayed the strongest induction by UV-B (log2 = 2.41), but three FPGAs were found within Cluster II (_FFT_, _CHI_, and _UGT78D2_), while the _4 CL3_ was not detected in this data set. Instead, several lignin pathway genes (LPGs), such as _CAD2/3/6/7/9_, _LAC17_, and _F5H2_ were assigned to Cluster I being suppressed by all three treatments. The only general phenylpropanol pathway gene (GPP) found in Cluster I is the _PAL3_ (phenylalanine ammonialylase), being indicative of metabolite channeling established during evolution by gene duplication [33].