Supercoiling of an excised genomic island represses effector gene expression to prevent activation of host resistance.

Abstract:

: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.

journal_name

Mol Microbiol

journal_title

Molecular microbiology

authors

Neale HC,Jackson RW,Preston GM,Arnold DL

doi

10.1111/mmi.14111

subject

Has Abstract

pub_date

2018-11-01 00:00:00

pages

444-454

issue

3

eissn

0950-382X

issn

1365-2958

journal_volume

110

pub_type

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