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Summary: The plant pathogen Pseudomonas syringae pv. phaseolicola, which causes halo blight disease of beans, contains a 106 kb genomic island PPHGI‐1. PPHGI‐1 carries a gene, avrPphB, which encodes an effector protein that triggers a resistance response in certain bean cultivars. Previous studies have shown that when PPHGI‐1 is excised from the bacterial chromosome, avrPphB is downregulated and therefore the pathogen avoids triggering the host's defence mechanism. Here, we investigate whether the downregulation of avrPphB is caused by the supercoiling of PPHGI‐1. We also investigate the effect of a PPHGI‐1‐encoded type 1A topoisomerase, TopB3, on island stability and bacterial pathogenicity in the plant. Supercoiling inhibitors significantly increased the expression of avrPphB but did not affect the excision of PPHGI‐1. An insertional mutant of topB3 displayed an increase in avrPphB expression and an increase in PPHGI‐1 excision as well as reduced population growth in resistant and susceptible cultivars of bean. These results suggest an important role for topoisomerases in the maintenance and stability of a bacterial‐encoded genomic island and demonstrate that supercoiling is involved in the downregulation of an effector gene once the island has been excised, allowing the pathogen to prevent further activation of the host defence response. The plant pathogen Pseudomonas syringae pv. phaseolicola contains a 106 kb genomic island designated PPHGI‐1. Here, we investigated the effect of supercoiling inhibitors on the expression of genes found on PPHGI‐1 and find that increasing the concentration of novobiocin relaxes the supercoiling of PPHGI‐1 when it is excised from the chromosome and that this allows increased expression of an island‐encoded effector gene. [ABSTRACT FROM AUTHOR]