Transcriptional repression of light‐induced flavonoid synthesis by elicitor treatment of cultured parsley cells

Abstract

Summary Cultured parsley (Petroselinum crispum) cells respond differentially to UV‐containing white light and fungal elicitor. Both stimuli activate the transcription of genes encoding enzymes of partly overlapping phenylpropanoid biosynthetic pathways. Irradiation induces vacuolar accumulation of flavonoids, whereas elicitor treatment stimulates the secretion of furanocoumarins. Simultaneous treatment of parsley cells with UV light and elicitor results in quantitative changes in both responses. Irradiation reduces elicitor‐induced furanocoumarin synthesis, possibly by post‐transcriptional mechanisms, whereas elicitor treatment completely blocks the light‐induced accumulation of flavonoids by repressing the transcription of the chalcone synthase gene. We have identified elicitor‐sensitive regions in the chalcone synthase promoter by transient expression analysis of selected promoter constructs linked to the β‐D‐glucuronidase reporter gene in parsley protoplasts. These regions are identical to those that were found to be sufficient for light inducibility of the chalcone synthase promoter.

Genome-wide analysis of the grapevine stilbene synthase multigenic family: genomic organization and expression profiles upon biotic and abiotic stresses

“…This is particularly true for the flavonoid pathway, which has been shown to be suppressed in a number of different plant species following exposure to fungal pathogens or fungal elicitors [91-94]. Recently Schenke et al [95] demonstrated that the induction of biosynthetic pathways, in Arabidopsis, responsible for the synthesis of lignin and the phytoalexin scopoletin, by the bacterial elicitor flg22, was associated with a strong suppression of flavonol biosynthesis genes including CHS.…”

UV-B damage and protection at the molecular level in plants

“…Chalcone synthase, for example, is transcriptionally activated by UV but not by fungal elicitor . Interestingly, treatment of cultured parsley cells with fungal elicitors strongly inhibited transcription of the CHS gene and blocked its UV-B induction, whereas gene expression for the general phenylpropanoid pathway was induced (Lozoya et al 1991). Since treatment with a fungal elicitor gives rise to secretion of furanocoumarins, which are also synthesized from intermediates of the phenylpropanoid pathway, the repression of the CHS gene is almost certainly a means for abolishing the drainage of precursors for coumarin synthesis through the flavonoid biosynthetic pathway.…”

“…Since treatment with a fungal elicitor gives rise to secretion of furanocoumarins, which are also synthesized from intermediates of the phenylpropanoid pathway, the repression of the CHS gene is almost certainly a means for abolishing the drainage of precursors for coumarin synthesis through the flavonoid biosynthetic pathway. By performing expression studies with different CHS promoter constructs involving the c/s-acting units, it has been shown that the same elements are involved in the down-regulation of CHS gene expression by a fungal elicitor (Lozoya et al 1991), probably by the binding of an elicitor-induced tram-acting factor which possesses a repressive function.…”

Suppression of UV‐B stress responses by flg22 is regulated at the chromatin level via histone modification

“…Given the fact that elicitor treatment can also shut down the UV‐B‐induced activation of the CHS gene expression if applied hours after UV‐B onset (Lozoya et al . ), we believe that both scenarios contribute to a deacetylated H3K9 state: removal of acetyl‐groups by HDAC activity in combination with prevention of re‐acetylation by suppressing HAT recruiting TFs. These two possibilities are now included in our updated working model presented in Fig.…”