INVESTIGADORES
GARRIZ Andres
congresos y reuniones científicas
Título:
Botrydial causes host cell death by inducing the hypersensitive response and by interacting with host signaling pathways that mediate defense responses against pathogens
Autor/es:
FRANCO R. ROSSI; ANDRÉS GÁRRIZ; MARÍA MARINA; MATÍAS F. ROMERO; MARÍA E. GONZALEZ; ISIDRO G. COLLADO ; FERNANDO L. PIECKENSTAIN
Lugar:
Cadiz
Reunión:
Congreso; XV International Botrytis Symposium; 2010
Institución organizadora:
Universidad de Cadiz
Resumen:
Necrotrophic plant pathogens such as B. cinerea kill host tissues and feed on the remains. B. cinereasecretes a variety of nonspecific phytotoxic metabolites that provoke host cell death. Amongthem, the tricyclic sesquiterpene botrydial is known to be toxic to several plant hosts and seemsto act as a strain-specific virulence factor.The hypersensitive response (HR), almost universally accepted as a form of programmedcell death, is typically triggered upon recognition of a pathogen-encoded avirulence protein by aresistance protein of the host plant. This response provides resistance to biotrophic pathogens byrestricting their access to living tissues. However, the HR enhances virulence of necrotrophicpathogens, by increasing tissue damage. In fact, B. cinerea is able to promote the host HR andthus takes advantage of this cell death process. Moreover, it has been proposed that HRinduction by B. cinerea is mediated by elicitors that act as virulence factors. However, the identityof such HR elicitors has not been clearly established. The aim of this work was to determine ifthe well-known sesquiterpene botrydial produced by B. cinerea merely acts as a ‘plain toxin’ or if,on the contrary, is able to induce the host HR.For this purpose, biochemical and molecular indicators of the HR were analysed onleaves of the model plant Arabidopsis thaliana treated with botrydial. Aniline-blue staining andepifluorescense microscopy revealed that botrydial induced callose deposition as early as 3 h aftertreatment (a.t.), this effect being more noticeable 24 h a.t. Autofluorescence analysis of leavestreated with botrydial revealed that this toxin also induced the accumulation of phenoliccompounds in host tissues, as evaluated both 3 and 24 h a.t.. Moreover, rapid accumulation ofreactive oxygen species in botrydial–treated leaves was evidenced by the redox-sensitive dyedihydrofluorescein diacetate. In addition to the above-mentioned biochemical markers of theHR, botrydial was found to cause a rapid and transient increase in mRNA levels of Athsr3 Thisgene is known to be induced early during the HR of A. thaliana elicited by pathogen attack and isconsidered as a molecular marker of the HR . In this way, it can be concluded that botrydial isable to induce the HR in plant tissues, this tricyclic sesquiterpene probably being one of theeffectors involved in HR elicitation by B. cinerea on its hosts.Additional evidence that botrydial is not a ‘plain toxin’ and that depends on host cellmachinery to exert its toxicity was obtained by analyzing the effects of botrydial on geneticallymodified plants affected in signaling pathways mediated by salicylic acid and jasmonic acid.Botrydial caused an increase in mRNA levels of PR1 and PDF1.2, two pathogenesis relatedproteins whose expression is respectively mediated by salicylic acid and jasmonic acid signaling.In addition, A. thaliana and tobacco (Nicotiana tabacum) plants defective in salicylic acid signalingwere more resistant to botrydial than wild type plants. On the contrary, and interestingly, A.thaliana plants defective in jasmonic acid signaling were more sensitive than wild type plants tobotrydial toxicity. Thus, botrydial toxicity was found to depend on host signaling pathwaysmediated by salicylic acid and jasmonic acid, both hormones seeming to play opposed roles inthe development of host cell death induced by this toxin.