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Xanthomonas campestris  pv.  campestris  ( Xcc ) is the causal agent of black rot of cruciferous plants, which harbor high levels of hydroxycinnamic acids (HCAs) in their above-ground parts. Thus, upon infection of the host plant, the pathogen experiences a complex cocktail of HCAs. The present study shows that  Xcc  can efficiently degrade the HCAs, 4-hydroxycinnamic acid (4-HCA), ferulic acid (FA) and sinapic acid (SiA), via an  hca  cluster which encodes putative genes for a 4-hydroxycinnamoyl-CoA synthetase/4-HCA ligase HcaL, a benzaldehyde dehydrogenase HcaD, a 4-hydroxycinnamoyl-CoA hydratase/lyase HcaH and a member of the MarR-family of transcriptional factors, HcaR.  Xcc  also degrades the HCA caffeic acid, but with an alternative mechanism. RT-PCR and subsequent GUS assays show that the  hca  cluster is transcribed within a single operon, and its transcription is specifically induced by 4-HCA, FA and SiA. Furthermore, we show that HcaR negatively regulates  hca  transcription when its ligand, the proposed degradation pathway intermediate HCA-CoA, is not present. HcaR specifically binds to a 25-bp site, which encompasses the -10 elements of the  hca  promoter. Finally, GUS histochemical staining and subsequent quantitative analysis shows that the  hca  cluster is transcribed  in planta  during pathogenesis of Chinese radish, and  hca  deletion mutant strains exhibit compromised virulence in cabbage. Together, these results suggest that the ability to degrade HCAs contributes to  Xcc  virulence by facilitating its growth and spread, and by protecting the pathogen from HCA toxicity. A working model to explain  Xcc  HCA sensing and subsequent induction of the HCA degradation process is proposed.

The phytopathogen Xanthomonas campestris scavenges hydroxycinnamic acids in planta via the hca cluster to increase virulence on its host plant