Wheat head blight caused by Gibberella zeae (anamorph: Fusarium graminearum) is a threat to food safety in China because of mycotoxin contamination of the harvested grain, the frequent occurrence of the disease, and the failure of chemical control in some areas due to benzimidazole resistance in the pathogen population. The molecular resistance mechanism, however, of G. zeae to benzimidazole fungicides (especially carbendazim; active ingredient: methyl benzimidazol-2-yl carbamate [MBC]) is poorly understood. DNA sequences of a beta-tubulin gene (beta(2)tub) (GenBank access number FG06611.1) in G. zeae were analyzed. Mutations in beta(2)tub in moderately resistant strains (MBC(MR)) included TTT (Phe)-->TAT (Tyr) at codon 167 or TTC (Phe)-->TAC (Tyr) at codon 200. A highly resistant strain (MBC(HR)) had two point mutations, one at codon 73, CAG (Gln)-->CGG (Arg), and the other at codon 198, GAG (Glu)-->CTG (Leu). To confirm that mutations in the beta(2)tub confer resistance to benzimidazole fungicides, the entire beta(2)tub locus was deleted from MBC(MR) and MBC(HR) strains of G. zeae. The resulting Deltabeta(2)tub mutants from both MBC(MR) and MBC(HR) strains grew normally on MBC-free potato dextrose agar medium and were supersensitive to MBC. Complementation of the Deltabeta(2)tub mutants by transformation with a copy of the intact beta(2)tub locus from their parent strains exhibited less resistance than the original strains, and complementation of the Deltabeta(2)tub mutants by transformation with a copy of the intact beta(2)tub locus from sensitive strains restored MBC sensitivity. The results indicated that the mutations in the beta(2)tub gene conferred resistance of G. zeae to benzimidazole fungicides and this gene can be used as a genetic marker in G. zeae.
Sclerotinia sclerotiorum is a devastating necrotrophic plant pathogen with a worldwide distribution. Cell wall-degrading enzymes and oxalic acid are important to the virulence of this pathogen. Here, we report a novel secretory protein, Ss-Rhs1, which is essential for the virulence of S. sclerotiorum. Ss-Rhs1 is believed to contain a typical signal peptide at the N-terminal and eight rearrangement hotspot (Rhs) repeats. Ss-Rhs1 exhibited a high level of expression at the initial stage of sclerotial development, as well as during the hyphal infection process. Targeted silencing of Ss-Rhs1 resulted in abnormal colony morphology and reduced virulence on host plants. Microscopic observations indicated that Ss-Rhs1-silenced strains exhibited reduced efficiency in compound appressoria formation.
Sclerotinia sclerotiorum (Lib.) de Bary is a devastating fungal pathogen with worldwide distribution. S. sclerotiorum is a necrotrophic fungus that secretes many cell wall-degrading enzymes (CWDEs) that destroy plant’s cell-wall components. Functional analyses of the genes that encode CWDEs will help explain the mechanisms of growth and pathogenicity of S. sclerotiorum. Here, we isolated and characterized a gene SsXyl1 that encoded an endo-β-1, 4-xylanase in S. sclerotiorum. The SsXyl1 expression showed a slight increase during the development and germination stages of sclerotia and a dramatic increase during infection. The expression of SsXyl1 was induced by xylan. The SsXyl1 deletion strains produce aberrant sclerotia that could not germinate to form apothecia. The SsXyl1 deletion strains also lost virulence to the hosts. This study demonstrates the important roles of endo-β-1, 4-xylanase in the growth and virulence of S. sclerotiorum.
Gummy stem blight (GSB), caused by Didymella bryoniae, is a devastating disease on watermelon.
Pydiflumetofen belongs
to succinate dehydrogenase inhibitor (SDHI) fungicide, which is effective
in controlling many plant diseases. The EC50 values of
69 D. bryoniae isolates to pydiflumetofen
ranged from 0.0018 to 0.0071 μg/mL, and the minimal inhibitory
concentration (MIC) value of all strains to pydiflumetofen was <0.05
μg/mL. Eight pydiflumetofen-resistant mutants were obtained,
and the level of resistance was stable. The mycelial growth, dry weight
of mycelia, hyphal morphology, and pathogenicity of most resistant
mutants did not change significantly compared with their parental
strains, which indicated that the resistance risk of D. bryoniae to pydiflumetofen would be medium to
high. Sequencing alignment showed that five resistant mutants presented
a mutation at codon 277 (H277Y) in the SdhB gene.
The point mutants FgSdhB
H248Y/R exhibited
decreased sensitivity to pydiflumetofen in Fusarium
graminearum, which indicated that the point mutants
of SdhB could reduce sensitivity to pydiflumetofen.
These results further increase our understanding about the mode of
action and the resistance mechanism of pydiflumetofen.
Summary
Sclerotinia sclerotiorum
is a devastating necrotrophic fungal pathogen that infects over 400 species of plants worldwide. Reactive oxygen species (ROS) modulations are critical for the pathogenic development of
S. sclerotiorum
. The fungus applies enzymatic and non‐enzymatic antioxidants to cope with the oxidative stress during the infection processes. Survival factor 1 was identified and characterized to promote survival under conditions of oxidative stress in
Saccharomyes cerevisiae
. In this research, a gene named
SsSvf1
was predicted to encode a survival factor 1 homologue in
S. sclerotiorum
.
SsSvf1
transcripts showed high expression levels in hyphae under oxidative stress. Silencing of
SsSvf1
resulted in increased sensitivity to oxidative stress in culture and increased levels of intracellular ROS. Transcripts of
SsSvf1
showed a dramatic increase during the initial stage of infection and the gene‐silenced strains displayed reduced virulence on oilseed rape and
Arabidopsis thaliana
. Inhibition of plant ROS production partially restores virulence of
SsSvf1
gene‐silenced strains.
SsSvf1
gene‐silenced strains exhibited normal oxalate production, but were impaired in compound appressorium formation and cell wall integrity. The results suggest that
SsSvf1
is involved in coping with ROS during fungal‐host interactions and plays a crucial role in the pathogenicity of
S. sclerotiorum
.
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