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Suppression of clubroot by C lonostachys rosea via antibiosis and induced host resistance
Author(s) -
Lahlali R.,
Peng G.
Publication year - 2014
Publication title -
plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.928
H-Index - 85
eISSN - 1365-3059
pISSN - 0032-0862
DOI - 10.1111/ppa.12112
Subject(s) - clubroot , jasmonic acid , biology , phenylpropanoid , antibiosis , canola , spore , botany , microbiology and biotechnology , horticulture , bacteria , brassica , biosynthesis , biochemistry , salicylic acid , gene , genetics
The mechanism of the biofungicide Prestop ® ( C lonostachys rosea ) was investigated for control of clubroot ( P lasmodiophora brassicae ) on canola. The key product components were partitioned and assessed for their effect on pathogen resting spores, root hair infection ( RHI ) and disease development using light microscopy, quantitative PCR and different application treatments during infection. The whole product of Prestop was consistently more effective than the C. rosea conidial suspension or product filtrate alone in reducing RHI and clubroot development. This biofungicide showed little effect on germination or viability of resting spores. Two‐application treatments at seeding and 7–14 days after seeding achieved greater clubroot control than a single application of the biofungicide at either seeding or post‐seeding stage. This may indicate the need to maintain a high biofungicide dose in the soil during primary and secondary infection. This biocontrol fungus colonized the rhizosphere and interior of canola roots extensively, and possibly induced plant resistance based on up‐regulation of the genes that are involved in jasmonic acid ( BnOPR2 ), ethylene ( BnACO ) and phenylpropanoid ( BnOPCL , BnCCR ) biosynthetic pathways. It is concluded that the biofungicide Prestop suppressed clubroot on canola at least via root colonization and induced systemic resistance ( ISR ), and the latter may be through the modulation of phenylpropanoid and jasmonic acid/ethylene metabolic pathways elicited by the fungus.