4.6 Article

The key iron assimilation genesClFTR1,ClNPS6were crucial for virulence ofCurvularia lunatavia initiating its appressorium formation and virulence factors

Journal

ENVIRONMENTAL MICROBIOLOGY
Volume 23, Issue 2, Pages 613-627

Publisher

WILEY
DOI: 10.1111/1462-2920.15101

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Funding

  1. National Natural Science Foundation of China [31271992]
  2. China Agriculture Research System [CARS-02-06]

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Iron is essential for all organisms and contributes to the virulence of plant pathogenic fungi. Two genes, ClFTR1 and ClNPS6, were identified in the maize pathogen Curvularia lunata, with significant roles in siderophore biosynthesis, oxidative stress mediation, and various stages of fungal development and infection. ClFTR1 regulates conidial germination and appressoria formation in the biotrophic phase, while ClNPS6 regulates toxin biosynthesis and enzyme activity in the necrotrophic phase, indicating their importance as key virulence factors in the pathogen.
Iron is virtually an essential nutrient for all organisms, to understand how iron contributes to virulence of plant pathogenic fungi, we identifiedClFTR1andClNPS6in maize pathogenCurvularia lunata(Cochliobolus lunatus) in this study. Disruption ofClNPS6significantly impaired siderophore biosynthesis.ClFTR1andClNPS6did mediate oxidative stress but had no significant impact on vegetative growth, conidiation, cell wall integrity and sexual reproduction. Conidial germination delayed and appressoria formation reduced in Delta Clftr1comparing with wild type (WT) CX-3. Genes responsible for conidial germination, appressoria formation, non-host selective toxin biosynthesis and cell wall degrading enzymes were also downregulated in the transcriptome of Delta Clftr1and Delta Clnps6compared with WT. The conidial development, toxin biosynthesis and polygalacturonase activity were impaired in the mutant strains withClFTR1andClNPS6deletion during their infection to maize.ClFTR1andClNPS6were upregulated expression at 12-24 and 48-120 hpi in WT respectively.ClFTR1positively regulated conidial germination, appressoria formation in the biotrophy-specific phase.ClNPS6positively regulates non-host selective toxin biosynthesis and cell wall degrading enzyme activity in the necrotrophy-specific phase. Our results indicated thatClFTR1andClNPS6were key genes of pathogen known to conidia development and virulence factors.

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