## 1 Introduction  
Plants respond to environmental cues with a plethora of induced defense reactions involving changes in secondary metabolite composition. In light of increased stress situations due to climate change, it is anticipated that combinations of abiotic and biotic stresses will pose a challenge to agricultural production. Therefore, it is important to understand the underlying molecular mechanisms of how plants perceive stress and integrate different stress signals in order to launch an appropriate defense to ensure survival. Revealing these mechanisms will allow the identification of suitable breeding targets to create stress-resilient crops. UV-B is a well-known inducer of flavonoid production. It is known for many years that this reaction is reliably suppressed during various plant-pathogen interactions. Infection can be mimicked by the elicitation with highly conserved elicitors, which are now termed microbial associated molecular patterns (MAMPs) [1]. This very stable crosstalk can be observed in many plant species and is therefore ideal to study mechanisms on how plants integrate different stress signals [2]. Plants exposed to both UV-B and pathogens/elicitors react with the suppression of UV-B-induced genes being involved in flavonoid production, regardless if MAMPs are applied concomitantly or after the onset of UV-B radiation [3; 4; 5; 6]. The binding of MAMPs to the receptor elicits the natural pathogen defense response of plants to pathogens termed pattern-triggered immunity (PTI). One MAMP which can be artificially synthesized is the proteinaceous flg22, a 22 amino acid peptide derived from the bacterial flagellin, which binds to the pattern recognition receptor FLS2 [7]. The key enzyme of the flavonoid-branch of the phenylpropanoid pathway (PP) is the chalcone synthase (CHS) constituting the entry point for flavonoid and subsequent anthocyanin production [8; 9] being strongly UV-B up-regulated and suppressed during PTI [5; 6; 10], and a perfect marker gene to investigate this crosstalk. The advantage lies in the re-distribution of resources and metabolic flow into other branches of the PP leading to the production of lignin and the coumarin phytoalexin scopoletin, components for a strong pathogen defense reaction [5]. In addition, PTI induced by flg22 goes along with strong up-regulation of _FRK1_, senescence, and flg22-induced receptor-like kinase, which can serve as a marker gene for successful plant treatment with this MAMP [11]. Plants require special protection against UV-B radiation because of their sessile nature and dependency on light. Strong UV-B radiation can damage membranes and organelles within the cell as well as DNA within the nucleus. The effect of UV-B radiation varies with the intensity and duration of irradiation and can directly or indirectly affect basic plant metabolic processes, such as respiration, photosynthesis, growth, and reproduction. At low doses as used in this study, UV-B light typically activates UV-B photoreceptor UV RESISTANCE LOCUS 8 (UVR8) [12], which will lead to a diversity of changes, such as the alternation of flowering time, reduction of hypocotyl growth, and biosynthesis of protective flavonoid metabolites [13]. In its inactive state, UVR8 forms a homodimer, which monomerizes upon UV-B perception and then translocates from the cytosol into the nucleus to interact with the E3 ubiquitin ligase COP1 [14], that is however regulated by white light [15]. In the nucleus UVR8-COP1 complex formation involves SPA1 (SUP-PRESSOR OF PHY A-105 1) and this can stabilize the bZIP transcription factor (TF) HY5 by preventing its degradation [14]. HY5 is a master-regulator of the photomorphogenic UV-B responses, including the production of flavonoids [16; 17]. A significant suppression of several structural genes in flavonoid biosynthesis was observed at 6 h, while at 3h the suppressing effect of flg22 was only visible by tendency, and later at 24h the effect was declining [5].