Publication | Open Access
Inactivation of<i>pqq</i>genes of<i>Enterobacter intermedium</i>60-2G reduces antifungal activity and induction of systemic resistance
48
Citations
23
References
2008
Year
Microbial PathogensPlant PathologyAntibiotic ResistanceBacterial PathogensPlant-pathogen InteractionDrug ResistanceMedical MicrobiologyBiosynthesisSystemic ResistanceSoft Rot PathogenInfection ControlAntimicrobial ResistanceHealth SciencesBiochemistryPlant-microbe InteractionGlucose DehydrogenaseHost-microbe InteractionClinical MicrobiologyPhosphate SolubilizationPlant ImmunityAntimicrobial Resistance GenePathogenesisMicrobiologyHost ResistanceMedicine
Enterobacter intermedium 60-2G, a phosphate solubilizing bacterium, has the ability to induce systemic resistance in plants against soft rot pathogen Erwinia carotovora. Glucose dehydrogenase, an enzyme that utilizes pyrroloquinoline quinone (PQQ) as a cofactor, is required for the synthesis of gluconic acid by E. intermedium 60-2G. Here, we report that the pqqA and pqqB genes are required for phosphate solubilization and induced systemic resistance against a soft rot pathogen in tobacco. Mutations in either the pqqA or pqqB gene abolished the production of 2-ketogluconic acid and eliminated the ability of E. intermedium to solubilize hydroxyapatite. Addition of gluconic acid to the growth media restored the ability of the pqqA mutant to produce 2-ketogluconic acid. Interestingly, both pqqA and pqqB mutants of E. intermedium lost their ability to inhibit the growth of the rice pathogen Magnaporthe grisea KI-409. Additionally, induced systemic resistance against the soft rot pathogen was attenuated in the pqq mutants. These functions were restored by complementation with the wild-type pqq gene cluster. Our findings suggest that PQQ plays an important function in beneficial traits including phosphate solubilization, antifungal activity, and induced systemic resistance of E. intermedium, possibly by acting as a cofactor for several enzymes including glucose dehydrogenase.
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