Phenylalanine increases chrysanthemum flower immunity against Botrytis cinerea attack
V Kumar, E Hatan, E Bar… - The Plant …, 2020 - Wiley Online Library
V Kumar, E Hatan, E Bar, R Davidovich‐Rikanati, A Doron‐Faigenboim, B Spitzer‐Rimon…
The Plant Journal, 2020•Wiley Online LibraryFlowers are the most vulnerable plant organ to infection by the necrotrophic fungus Botrytis
cinerea. Here we show that pre‐treatment of chrysanthemum (Chrysanthemum morifolium)
flowers with phenylalanine (Phe) significantly reduces their susceptibility to B. cinerea. To
comprehend how Phe treatment induces resistance, we monitored the dynamics of
metabolites (by GC/LC‐MS) and transcriptomes (by RNAseq) in flowers after Phe treatment
and B. cinerea infection. Phe treatment resulted in accumulation of 3‐phenyllactate and …
cinerea. Here we show that pre‐treatment of chrysanthemum (Chrysanthemum morifolium)
flowers with phenylalanine (Phe) significantly reduces their susceptibility to B. cinerea. To
comprehend how Phe treatment induces resistance, we monitored the dynamics of
metabolites (by GC/LC‐MS) and transcriptomes (by RNAseq) in flowers after Phe treatment
and B. cinerea infection. Phe treatment resulted in accumulation of 3‐phenyllactate and …
Summary
Flowers are the most vulnerable plant organ to infection by the necrotrophic fungus Botrytis cinerea. Here we show that pre‐treatment of chrysanthemum (Chrysanthemum morifolium) flowers with phenylalanine (Phe) significantly reduces their susceptibility to B. cinerea. To comprehend how Phe treatment induces resistance, we monitored the dynamics of metabolites (by GC/LC‐MS) and transcriptomes (by RNAseq) in flowers after Phe treatment and B. cinerea infection. Phe treatment resulted in accumulation of 3‐phenyllactate and benzaldehyde, and in particular induced the expression of genes related to Ca2+ signaling and receptor kinases, implicating an induction of the defense response. Interestingly, the main effects of Phe treatment were observed in flowers exposed to B. cinerea infection, stabilizing the global fluctuations in the levels of metabolites and transcripts while reducing susceptibility to the fungus. We suggest that Phe‐induced resistance is associated to cell priming, enabling rapid and targeted reprogramming of cellular defense responses to resist disease development. After Phe pre‐treatment, the levels of the anti‐fungal volatiles phenylacetaldehyde and eugenol were maintained and the level of coniferin, a plausible monolignol precursor in cell wall lignification, was strongly increased. In addition, Phe pre‐treatment reduced ROS generation, prevented ethylene emission, and caused changes in the expression of a minor number of genes related to cell wall biogenesis, encoding the RLK THESEUS1, or involved in Ca2+ and hormonal signaling processes. Our findings point to Phe pre‐treatment as a potential orchestrator of a broad‐spectrum defense response which may not only provide an ecologically friendly pest control strategy but also offers a promising way of priming plants to induce defense responses against B. cinerea.
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