Abstract
Several reports have recently contributed to determine the effector inventory of the sequenced strain Pseudomonas syringae pv. phaseolicola (Pph) 1448a. However, the contribution to virulence of most of these effectors remains to be established. Genetic analysis of the contribution to virulence of individual P. syringae effectors has been traditionally hindered by the lack of phenotypes of the corresponding knockout mutants, largely attributed to a high degree of functional redundancy within their effector inventories. In support of this notion, effectors from Pseudomonas syringae pv. tomato (Pto) DC3000 have been classified into redundant effector groups (REGs), analysing virulence of polymutants in the model plant Nicotiana benthamiana. However, using competitive index (CI) as a virulence assay, we were able to establish the individual contribution of AvrPto1Pto DC3000 to Pto DC3000 virulence in tomato, its natural host, even though typically, contribution to virulence of AvrPto1 is only shown in strains also lacking AvrPtoB (also called HopAB2), a member of its REG. This report raised the possibility that even effectors targeting the same defence signalling pathway may have an individual contribution to virulence, and pointed out to CI assays as the means to establish such a contribution for individual effectors. In this work, we have analysed the individual contribution to virulence of the majority of previously uncharacterised Pph 1448a effectors, by monitoring the development of disease symptoms and determining the CI of single knockout mutants at different stages of growth within bean, its natural host. Despite their potential functional redundancy, we have found individual contributions to virulence for six out of the fifteen effectors analysed. In addition, we have analysed the functional relationships between effectors displaying individual contribution to virulence, highlighting the diversity that these relationships may present, and the interest of analysing their functions within the context of the infection.
Highlights
Pseudomonas syringae is a gram-negative host-specific pathogen that depends on the Hrp type III secretion system (T3SS) to secrete and translocate effector proteins into the plant cell, causing disease in compatible hosts, and triggering a hypersensitive response (HR) in incompatible hosts [1]
DhopR1, displayed a sustained and reproducible reduction in the induction of disease symptoms in bean leaves whereas the rest either displayed no differences with the wild type strain, or differences too subtle or variable to be established with confidence (Table 2 and Figure 1)
The individual contribution of T3SS effectors to virulence has been traditionally difficult to establish in P. syringae, a fact usually explained by the redundant activities reported for several functionally characterized effectors [3,4,5,6,7]
Summary
Pseudomonas syringae is a gram-negative host-specific pathogen that depends on the Hrp type III secretion system (T3SS) to secrete and translocate effector proteins into the plant cell, causing disease in compatible hosts, and triggering a hypersensitive response (HR) in incompatible hosts [1]. Functional redundancy between effectors has been repeatedly proposed as the determining factor hindering the detection of virulence phenotypes for single effector mutants. In support of this notion, functional characterisation has already revealed seemingly similar defence suppressing capabilities for many P. syringae effectors [11]. In some cases, such as that of effectors AvrPto and AvrPtoB ( called HopAB2) from P. syringae pv. Virulence assays with higher sensitivity than standard assays, i.e. competitive index assays (CIs), have allowed detection of virulence phenotypes for single effector mutants such as AvrPto1 [15,16]
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