Insect eggs induce a systemic acquired resistance against Botrytis cinerea

Détails

Ressource 1Télécharger: thèse-OK.pdf (19070.56 [Ko])
Etat: Public
Version: Après imprimatur
Licence: Non spécifiée
ID Serval
serval:BIB_73FFDE94D9D8
Type
Thèse: thèse de doctorat.
Collection
Publications
Institution
Titre
Insect eggs induce a systemic acquired resistance against Botrytis cinerea
Auteur⸱e⸱s
ALFONSO Esteban
Directeur⸱rice⸱s
Reymond Philippe
Détails de l'institution
Université de Lausanne, Faculté de biologie et médecine
Statut éditorial
Acceptée
Date de publication
2021
Langue
anglais
Résumé
Despite their inert stage, insect eggs deposited on leaves represent a considerable threat since they will develop into feeding larvae. Plants respond actively to insect eggs deposition by triggering various defenses that lead to egg desiccation, drop-off, mortality, or attraction of egg parasitoids. Upon Pieris brassicae oviposition, Arabidopsis thaliana activates the salicylic acid (SA) pathway, which is usually induced to fend off bacterial pathogens. Recently, it was shown that P. brassicae oviposition and treatment with egg extract (EE) induce a systemic acquired resistance (SAR) against the bacterial pathogen Pseudomonas syringae in A. thaliana. The aim of this thesis was to investigate whether egg-induced SAR was also effective against the fungal necrotroph Botrytis cinerea.
Here, we show that P. brassicae oviposition and EE treatment induce SAR against B. cinerea. This effect was reproducible when plants were treated with EE from the generalist Spodoptera littoralis. Furthermore, pretreatment with a solution of phosphatidylcholines, which are active compounds found in P. brassicae and S. littoralis eggs, reduced B. cinerea growth to the same extent as EE. This indicates that egg-induced SAR is triggered following perception of an egg-associated molecular pattern. EE-induced SAR is abolished in ics1, ald1 and fmo1 mutants, indicating that the SA and N-hydroxy-pipecolic acid pathways are involved. In addition, we found that EE-induced SAR establishment requires tryptophan-derived metabolites, with a substantial contribution of camalexin, a known antifungal compound. Indeed, we found that SAR is abolished in several mutants deficient in camalexin biosynthesis, including cyp79b2 cyp79b3, cyp71a12 cyp71a13, pad3-1 and wrky33. Although we found that expression of the camalexin biosynthesis gene PAD3 is primed by EE treatment, metabolic analyses revealed that levels of camalexin are not different between control and EE-treated plants, leaving open the question on how camalexin exerts its action. Finally, we found that EE treatment also reduced infection by an oomycete pathogen, illustrating the broad range activity of EE-induced SAR.
We also demonstrate that P. brassicae larvae performance is reduced in B. cinerea- infected plants, which implies that egg-induced SAR might benefit the insect. This phenomenon might illustrate a strategy of the insect that manipulates plant SA pathway through oviposition to reduce pathogen infections that are detrimental for future hatching larvae.
Création de la notice
30/09/2021 11:15
Dernière modification de la notice
08/10/2021 6:10
Données d'usage