Abstract
Pseudomonas syringae pv. phaseolicola is the causative agent of halo blight in the common bean, Phaseolus vulgaris. P. syringae pv. phaseolicola race 4 strain 1302A contains the avirulence gene avrPphB (syn. hopAR1), which resides on PPHGI-1, a 106 kb genomic island. Loss of PPHGI-1 from P. syringae pv. phaseolicola 1302A following exposure to the hypersensitive resistance response (HR) leads to the evolution of strains with altered virulence. Here we have used fluorescent protein reporter systems to gain insight into the mobility of PPHGI-1. Confocal imaging of dual-labelled P. syringae pv. phaseolicola 1302A strain, F532 (dsRFP in chromosome and eGFP in PPHGI-1), revealed loss of PPHGI-1::eGFP encoded fluorescence during plant infection and when grown in vitro on extracted leaf apoplastic fluids. Fluorescence-activated cell sorting (FACS) of fluorescent and non-fluorescent PPHGI-1::eGFP F532 populations showed that cells lost fluorescence not only when the GI was deleted, but also when it had excised and was present as a circular episome. In addition to reduced expression of eGFP, quantitative PCR on sub-populations separated by FACS showed that transcription of other genes on PPHGI-1 (avrPphB and xerC) was also greatly reduced in F532 cells harbouring the excised PPHGI-1::eGFP episome. Our results show how virulence determinants located on mobile pathogenicity islands may be hidden from detection by host surveillance systems through the suppression of gene expression in the episomal state.
Highlights
The exchange of genomic pathogenicity islands by horizontal gene transfer is recognised as a key factor in the development of new more virulent bacterial pathogens of both animals and plants [1,2,3,4]
We study the mobility of an island named PPHGI-1 in Pseudomonas syringae pv. phaseolicola that causes halo-blight disease of bean
The exposure of P. syringae pv. phaseolicola to plant defenses triggers the excision of PPHGI-1, creation of a circular episomal form and deletion of the genomic island (GI) or its transfer to other bacteria
Summary
The exchange of genomic pathogenicity islands by horizontal gene transfer is recognised as a key factor in the development of new more virulent bacterial pathogens of both animals and plants [1,2,3,4]. The primary mechanism of plant resistance against P. syringae is a basal defense response that is induced upon detection of conserved microbe associated molecular patterns (MAMPS) [10]. Pathovars of P. syringae are able to overcome MAMP triggered defense by delivering into the plant cytoplasm an array of effector proteins that inactivate surveillance mechanisms and signal transduction pathways, thereby allowing bacterial multiplication [11,12,13]. Many plants have evolved resistance proteins that recognise a subset of these effector proteins, termed avirulence (Avr) proteins, which trigger a hypersensitive resistance response (HR) leading to programmed cell death at infection sites and the restriction of colonisation [14,10]
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