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Microbes and EnvironmentsPlant BiologyPeer-reviewed journal article

Induced systemic resistance by the root colonization of Trichoderma atroviride is independent from the chitin-mediated signaling pathway in Arabidopsis

Ayae Sakai, Hisako Yamagata, Keigo Naito, Mai Yoshioka, Takaya TominagaiD, Shinsuke IfukuiD, Hironori KaminakaiD

PDFDOIPreprint

Abstract

Beneficial root endophytic fungi induce systemic responses, growth promotion, and induced systemic resistance (ISR) in the colonized host plants. Soil application of chitin, a main component of fungal cell walls, also systemically induces disease resistance. Thus, chitin recognition and its downstream signaling pathway are supposed to mediate ISR triggered by beneficial fungi colonizing the root. This study compared systemic disease resistance and transcriptional responses induced by Trichoderma, a representative beneficial root endophytic fungus, and chitin in Arabidopsis. A significant plant growth promotion was observed under root colonization by the three tested beneficial fungi, Trichoderma atroviride, Serendipita indica, and S. vermifera. Still, only T. atroviride and S. indica triggered ISR against the necrotrophic fungal pathogen Alternaria brassicicola. Induced systemic resistance triggered by T. atroviride was compromised in the chitin-receptor mutant, while systemic resistance caused by soil application of chitin was not. Transcriptome analysis demonstrated that the chitin-regulated genes are mostly shared with those regulated by T. atroviride, but many of the latter were specific. However, the commonly enriched gene ontologies for those regulated genes indicated that T. atroviride inoculation and chitin application systemically control similar transcriptional responses, mainly associated with cell wall functions. Taken together, Trichoderma could trigger ISR primarily independently from the chitin-mediated signaling pathway; however, chitin and Trichoderma would systemically induce similar cellular functions in ISR aboveground.

Citations
8
FWCI
1.69
Field percentile
top 16%

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