Premium
Lack of the plant signalling component SGT1b enhances disease resistance to Fusarium culmorum in Arabidopsis buds and flowers
Author(s) -
Cuzick Alayne,
Maguire Kerry,
HammondKosack Kim E.
Publication year - 2009
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/j.1469-8137.2008.02712.x
Subject(s) - fusarium culmorum , arabidopsis , component (thermodynamics) , biology , resistance (ecology) , plant disease resistance , botany , signalling , fusarium , agronomy , gene , microbiology and biotechnology , genetics , mutant , physics , thermodynamics
Summary• Fusarium culmorum causes ear blight disease on cereal crops resulting in considerable losses to grain yield, quality and safety. This fungus can also infect Arabidopsis floral tissues. In this study, the Arabidopsis floral infection model was used to assess the impact of five defence mutants on disease. • Fusarium culmorum was spray inoculated onto the floral tissues of the mutants eds1 , lms1 , rar1 , sgt1a and sgt1b involved in basal and resistance gene‐mediated defence to pathogens. Floral disease development was assessed quantitatively. • Only the sgt1b mutant exhibited a significantly different interaction phenotype compared with wild‐type plants. The buds and flowers were more resistant to infection and developed milder symptoms, but had wild‐type levels of deoxynivalenol (DON) mycotoxin. Microscopic studies indicated that to cause disease, F. culmorum requires plant cells in the invaded tissues to be competent to activate both a cell death response and a sustained oxidative burst. The sgt1a mutant exhibited a weak trend towards greater disease resistance in the new silique tissues. • This study highlights that the SGT1‐mediated signalling cascade(s), which had previously only been demonstrated to be required for Arabidopsis resistance against biotrophic pathogens, is causally involved in F. culmorum disease symptom development.