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ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Sunflower and Plant Biology Research » Research » Publications at this Location » Publication #365256
Research Project: Sclerotinia Initiative

Location: Sunflower and Plant Biology Research

Title: Mechanisms of broad host range necrotrophic pathogenesis in Sclerontinia sclerotiorum

Author
item LIANG, XIAOFEI - UNIVERSITY OF FLORIDA
item ROLLINS, JEFFREY - UNIVERSITY OF FLORIDA

Submitted to: Phytopathology
Publication Type: Review Article
Publication Acceptance Date: 7/17/2018
Publication Date: 8/30/2018
Citation: Liang, X., Rollins, J.A. 2018. Mechanisms of broad host range necrotrophic pathogenesis in Sclerontinia sclerotiorum. Phytopathology. 108:1128-1140. https://doi.org/10.1094/PHYTO-06-18-0197-RVW.
DOI: https://doi.org/10.1094/PHYTO-06-18-0197-RVW

Interpretive Summary:

Technical Abstract: Among necrotrophic fungi, Sclerotinia sclerotiorum is remarkable for its extremely broad host range and for its aggressive host tissue colonization. With full genome sequencing, transcriptomic analyses and the increasing pace of functional gene characterization, the factors underlying the basis of this broad host range necrotrophic pathogenesis are now being elucidated at a greater pace. Among these, genes have been characterized that are required for infection via compound appressoria in addition to genes associated with colonization that regulate oxalic acid (OA) production and OA catabolism. Moreover, virulence-related secretory proteins have been identified, among which are candidates for manipulating host activities apoplastically and cytoplasmically. Coupled with these mechanistic studies, cytological observations of the colonization process have blurred the heretofore clear-cut biotroph versus necrotroph boundary. In this review, we reexamine the cytology of S. sclerotiorum infection and put more recent molecular and genomic data into the context of this cytology. We propose a two-phase infection model in which the pathogen first evades, counteracts and subverts host basal defense reactions prior to killing and degrading host cells. Spatially, the pathogen may achieve this via the production of compatibility factors/effectors in compound appressoria, bulbous subcuticular hyphae, and primary invasive hyphae. By examining the nuances of this interaction, we hope to illuminate new classes of factors as targets to improve our understanding of broad host range necrotrophic pathogens and provide the basis for understanding corresponding host resistance.