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A study on the molecular mechanism of resistance to amicarthiazol in Xanthomonas campestris pv. citri
Jun Li1, Mingguo Zhou, Hongxia Li
1College of Plant Protection, Nanjing Agricultural University, Nanjing 210095, China.
Abstract:
Three amicarthiazol-resistant mutants (Xuv10, Xuv20 and Xuv40) were obtained by UV induction and used in this study. Minimal inhibition concentrations (MICs) of amicarthiazol against the growth of mutants and wild-type isolate were 400 and 100 microg ml(-1) respectively. Inhibition by amicarthiazol of succinate dehydrogenase (SDH) activities of Xanthomonas campestris pv. citri (Hasse) Dye wild-type isolate (Xcc) and three resistant mutants derived from this isolate were assayed using triphenyltetrazolium chloride (TTC). The SDH activities of these mutants were significantly lower than that of Xcc. The complete nucleotide sequences of four subunits (SdhA, SdhB, SdhC and SdhD) of succinate-ubiquinone oxidoreductase (SQR) were cloned by polymerase chain reaction (PCR) amplification. An amino acid mutation (His229--> Leu229) in sdhB was found to confer resistance of X. campestris pv. citri to amicarthiazol. It is suggested that this mutation alters the SDH complex in some way that prevents binding of amicarthiazol.
Insights
Amicarthiazol resistance in Xanthomonas campestris pv. citri is linked to a mutation in the succinate dehydrogenase (SDH) enzyme. This specific amino acid change (His229--> Leu229) in the sdhB gene reduces enzyme activity and prevents amicarthiazol binding.
Area of Science:
- Plant Pathology
- Molecular Biology
- Biochemistry
Background:
- Xanthomonas campestris pv. citri (Xcc) causes citrus canker.
- Amicarthiazol is a potential fungicide targeting succinate dehydrogenase (SDH).
- Understanding resistance mechanisms is crucial for disease management.
Purpose of the Study:
- To investigate the molecular basis of amicarthiazol resistance in Xcc.
- To identify specific mutations conferring resistance.
- To elucidate the impact of these mutations on SDH function.
Main Methods:
- Induction of amicarthiazol-resistant mutants using UV radiation.
- Determination of minimal inhibition concentrations (MICs) for wild-type and mutant strains.
- Assay of succinate dehydrogenase (SDH) activity using triphenyltetrazolium chloride (TTC).
- Cloning and sequencing of SDH subunit genes (SdhA, SdhB, SdhC, SdhD) via PCR amplification.
Main Results:
- Three resistant mutants (Xuv10, Xuv20, Xuv40) showed significantly lower SDH activity compared to wild-type Xcc.
- MICs for mutants were 400 µg/mL, while wild-type was 100 µg/mL.
- A specific mutation (His229--> Leu229) was identified in the sdhB gene of resistant mutants.
Conclusions:
- The His229--> Leu229 mutation in the sdhB gene confers resistance to amicarthiazol in Xcc.
- This mutation likely alters the SDH complex structure, hindering amicarthiazol binding.
- The findings provide insights into fungicide resistance mechanisms in plant pathogens.
