Effects of capsidiol on the lipid and protein content of isolated membranes of Phytophthora capsici

Turelli, M.; Coulomb, Claude; Coulomb, P.; Roggero, Jean‐Pierre; Bounias, M.

doi:10.1016/0048-4059(84)90029-8

Cited by 12 publications

(7 citation statements)

References 17 publications

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“…Data are means 6 SE (n = 8). Data marked with asterisks are significantly different as assessed by two-tailed Student's t tests: **P < 0.01. terpenoids, and alkaloids, are produced by different plant families (Hammerschmidt, 1999), it is generally considered that phytoalexins act by inducing changes in permeability of fungal, oomycete, and bacterial cellular membranes (Smith, 1982;Turelli et al, 1984;Robertson et al, 1985). Phytoalexin toxicity is not specific to microorganisms but is also destructive to plant cells (Shiraishi et al, 1975;Smith, 1982).…”

Section: Discussionmentioning

confidence: 99%

The Full-Size ABCG Transporters Nb-ABCG1 and Nb-ABCG2 Function in Pre- and Postinvasion Defense against Phytophthora infestans in Nicotiana benthamiana

et al. 2016

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Section: Discussionmentioning

confidence: 99%

The Full-Size ABCG Transporters Nb-ABCG1 and Nb-ABCG2 Function in Pre- and Postinvasion Defense against Phytophthora infestans in Nicotiana benthamiana

et al. 2016

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“…Silencing of NbEAS or NbEAH increases the susceptibility of the host N. benthamiana to P. infestans , supporting the defensive role of capsidiol. Finally, capsidiol exhibits fungistatic activity on many fungal species by inhibiting mycelial growth and zoospore germination (Ward et al ., ; Bailey et al ., ; Turelli et al ., ). Nonetheless, nonadapted P. infestans is at least 10 times more sensitive to capsidiol than adapted P. capsici (Jones et al ., ; Giannakopoulou et al ., ), which suggests that P. infestans has not evolved a mechanism to overcome capsidiol antifungal activity, and capsidiol plays an important role in pepper NHR against P. infestans (Lee et al ., ).…”

Section: Introductionmentioning

confidence: 97%

Expansion of sesquiterpene biosynthetic gene clusters in pepper confers nonhost resistance to the Irish potato famine pathogen

Lee

Kim

et al. 2017

New Phytologist

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Chemical barriers contribute to nonhost resistance, which is defined as the resistance of an entire plant species to nonadapted pathogen species. However, the molecular basis of metabolic defense in nonhost resistance remains elusive. Here, we report genetic evidence for the essential role of phytoalexin capsidiol in nonhost resistance of pepper (Capsicum spp.) to potato late blight Phytophthora infestans using transcriptome and genome analyses. Two different genes for capsidiol biosynthesis, 5-epi-aristolochene synthase (EAS) and 5-epi-aristolochene-1,3-dihydroxylase (EAH), belong to multigene families. However, only a subset of EAS/EAH gene family members were highly induced upon P. infestans infection, which was associated with parallel accumulation of capsidiol in P. infestans-infected pepper. Silencing of EAS homologs in pepper resulted in a significant decrease in capsidiol accumulation and allowed the growth of nonadapted P. infestans that is highly sensitive to capsidiol. Phylogenetic and genomic analyses of EAS/EAH multigene families revealed that the emergence of pathogen-inducible EAS/EAH genes in Capsicum-specific genomic regions rendered pepper a nonhost of P. infestans. This study provides insights into evolutionary aspects of nonhost resistance based on the combination of a species-specific phytoalexin and sensitivity of nonadapted pathogens.

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“…The second scenario would be that B. cinerea recognizes the damage caused by phytoalexins. However, as for capsidiol and rishitin, both are presumed to have cell membranes as their targets, and these phytoalexins are relatively unspecific toxicants that cause damage even to plant cells (5, 13, 17, 45), so it is not certain whether there exists a specific target by which these two compounds can be distinguished. Given that some genes, such as BcatrB encoding a multidrug resistance pump, are commonly induced by structurally unrelated phytoalexins and fungicides treatments (26, 27), B. cinerea may possess both induction mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Botrytis cinerea identifies host plants via the recognition of antifungal capsidiol to induce expression of a specific detoxification gene

Kuroyanagi

Bulasag

Fukushima

et al. 2022

Preprint

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The gray mold pathogen Botrytis cinerea has a broad host range, causing disease in over 400 plant species, but it is not known how this pathogen evolved this polyxenous nature. B. cinerea can metabolize a wide range of phytoalexins, including the stilbenoid, resveratrol, and the sesquiterpenoids capsidiol in tobacco, and rishitin in potato and tomato. In this study, we analyzed the metabolism of sesquiterpenoid phytoalexins by B. cinerea. Capsidiol was dehydrogenated to capsenone which was then further oxidized, while rishitin was directly oxidized to epoxy- or hydroxy-rishitins indicating that B. cinerea has separate mechanisms to detoxify structurally similar sesquiterpenoid phytoalexins. RNAseq analysis revealed that a distinct set of genes were induced in B. cinerea when treated with capsidiol or rishitin, suggesting that B. cinerea can distinguish structurally similar phytoalexins to activate appropriate detoxification mechanisms. The gene most highly upregulated by capsidiol treatment encoded a dehydrogenase, designated Bccpdh. Heterologous expression of Bccpdh in a capsidiol-sensitive plant symbiotic fungus, Epichloë festucae, resulted in an acquired tolerance of capsidiol and the ability to metabolize capsidiol to capsenone, while B. cinerea Δbccpdh mutants became relatively sensitive to capsidiol. The Δbccpdh mutant showed reduced virulence on the capsidiol producing Nicotiana and Capsicum species but remained fully pathogenic on potato and tomato. Homologs of Bccpdh are found in taxonomically distant Ascomycota fungi but not in other Botrytis species, suggesting that B. cinerea acquired the ancestral Bccpdh by horizontal gene transfer, thereby extending the pathogenic host range of this polyxenous pathogen to capsidiol-producing plant species.Significance StatementB. cinerea can metabolize a wide range of phytoalexins, however, the extent to which phytoalexin detoxification contributes to pathogenicity is largely unknown. In this study, we have shown that B. cinerea recognizes structurally resembling sesquiterpenoid phytoalexins, rishitin and capsidiol, to activate appropriate detoxification mechanisms. We identify Bccpdh, encoding a dehydrogenase for capsidiol detoxification, which is upregulated in B. cinerea exclusively during the infection of capsidiol producing plant species, and is required to exert full virulence. Analysis of the Bccpdh locus suggests that the gene was acquired via horizontal gene transfer. This work highlights that the polyxenous plant pathogen B. cinerea can distinguish its host plants by its anti-microbial compounds, to activate appropriate mechanisms for enhanced virulence.

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Effects of capsidiol on the lipid and protein content of isolated membranes of Phytophthora capsici

Cited by 12 publications

References 17 publications

The Full-Size ABCG Transporters Nb-ABCG1 and Nb-ABCG2 Function in Pre- and Postinvasion Defense against Phytophthora infestans in Nicotiana benthamiana

The Full-Size ABCG Transporters Nb-ABCG1 and Nb-ABCG2 Function in Pre- and Postinvasion Defense against Phytophthora infestans in Nicotiana benthamiana

Expansion of sesquiterpene biosynthetic gene clusters in pepper confers nonhost resistance to the Irish potato famine pathogen

Botrytis cinerea identifies host plants via the recognition of antifungal capsidiol to induce expression of a specific detoxification gene

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