4.7 Article

Lilium Gray Mold Suppression Conferred by the Host Antimicrobial Protein LsGRP1 Involves Main Pathogen-Targeted Manipulation of the Nonantimicrobial Region LsGRP1(N)

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Publisher

AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.3c04221

Keywords

antimicrobial sensitivity; pathogen manipulation; spore germination; hyphal growth; infection-relatedgene expression; host defense elicitation; Botrytis elliptica

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Antimicrobial protein LsGRP1 protects Lilium from gray mold caused by Botrytis elliptica, but its nonantimicrobial region LsGRP1(N) promotes spore germination of the fungus. By testing the effects of LsGRP1(N), LsGRP1, and the combination of LsGRP1(N) and the antimicrobial region LsGRP1(C), it was found that LsGRP1(N) enhances the sensitivity of B. elliptica to LsGRP1(C) and suppresses disease development. LsGRP1(N) also reduces gene expression related to B. elliptica infection and increases host defense activity.
Antimicrobial protein LsGRP1 protects Lilium from gray mold mainly caused by the destructive pathogen Botrytis elliptica; however, its nonantimicrobial region LsGRP1(N) conversely promotes spore germination of this fungus. By assaying the effects of LsGRP1(N), LsGRP1, and the combination of LsGRP1(N) and the antimicrobial region LsGRP1(C) on fungal spore germination, hyphal growth, and Lilium gray mold development, LsGRP1(N) was found to improve the LsGRP1(C) sensitivity of B. elliptica and disease suppression by LsGRP1(C). B. elliptica cell vitality assays indicated that LsGRP1(N) pretreatment uniquely enhanced the lethal efficiency of LsGRP1(C) compared to the control peptides. In addition, LsGRP1(N)-treated B. elliptica was demonstrated to lower infection-related gene expression and increase host-defense-eliciting activity, as indicated by reverse transcription quantitative polymerase chain reaction and histochemical-staining-based callose detection results, respectively. Therefore, LsGRP1(N) showed a novel mode of action for antimicrobial proteins by manipulating the main pathogen, which facilitated the development of targetspecific and dormant microbe-eradicating antimicrobial agents.

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