Disrupting the quorum sensing mediated virulence in soft rot causing Pectobacterium carotovorum by marine sponge associated Bacillus sp. OA10

Strains of genus Pectobacterium are major cause of soft rot diseases in fruits and vegetables worldwide. Traditional control methods have not been very successful in combating the pathogenesis. As a result there has been an emerging need for developing an alternative ecofriendly and economical strategy. The pathogenesis of Pectobacterium sp. is mediated by quorum sensing (QS) and approaches based on inhibition of QS system to shut down the virulence genes without affecting growth of the pathogen may serve the purpose. Bacillus sp. OA10 associated with purple sponge Haliclona sp. was found to possess extracellular quorum quenching activity. The OA10 extract inhibited QS dependent virulence of Pectobacterium carotovorum subsp. carotovorum BR1 (PccBR1) at low concentrations (0.2 mg) as evident from 77.56 +/- 6.17% reduction in potato maceration with complete inhibition by 0.8 mg. Inhibition of plant cell wall degrading enzymes (PCWDE) and carbapenem production by PccBR1 in presence of OA10 extract indicated disruption of the two QS pathways ExpI/ExpR and CarI/CarR in PccBR1. Bacillus sp. OA10 was not found to degrade acyl homoserine lactone (AHL), instead exhibited QSI activity by probably inhibiting AHL synthesis in PccBR1. Absence of enzymatic principle in quorum sensing inhibitor (QSI) is beneficial as enzymes may get inhibited by various factors during their application. OA10 extract did not affect growth of PccBR1, thereby reducing the chance of developing resistance against the QSI. Thus, Bacillus sp. OA10 can prove to be a good prospective candidate for QSI based novel biocontrol formulations.

Automated summary

Genus Pectobacterium is a major cause of soft rot diseases in fruits and vegetables globally, and there is a need for alternative ecofriendly and economical strategies. Bacillus sp. OA10 extract can effectively inhibit the pathogenicity of PccBR1, potentially by disrupting the QS pathways.