Student of the Month (April 2009)
Name: Christopher Clarke (gtg681r at vt.edu)
Research project: Dissecting the molecular basis of pathogenicity for the phytopathogen Pseudomonas syringae: From general pathogenicity to host adaptation.
Advisor: Boris Vinatzer
Departmental affiliation: PPWS
Anticipated defense date: 2012
Project description:
Peudomonas syringae is a pathogen of many different plant species, but any given strain of
P. syringae is a pathogen of only a few plants. P. syringae is a sophisticated
pathogen able to subvert many known plant defense responses by secreting effector proteins through
its Type III Secretion System encoded by the hrp/hrc gene cluster. The first part of my
project involves characterizing a subgroup of P. syringae strains that lack the canonical
Type III Secretion System. Members of this novel group are commonly found on healthy plants and
do not appear to cause disease symptoms on a diverse variety of tested plants. They do, however,
have an atypical Type III Secretion System and a few effectors of the P. syringae metagenome
and a few novel effectors. Thus, these strains appear to represent common epiphytic bacteria on the
verge of phytopathogenicity. The molecular basis of general pathogenicity of P. syringae may
be further elucidated by comparing this group of strains to the typical P. syringae pathogens.
Additionally, these strains have orthologues to several toxins and effectors that contribute to
pathogenicity of insects, likely indicating that the host range of P. syringae transcends the plant kingdom.
The second part of my project revolves around an ongoing effort to characterize the molecular determinants
that define the host range of any specific P. syringae strain. The Vinatzer lab is developing a model
system for nonhost resistance that involves two closely related P. syringae pathogens: a tomato and
Arabidopsis pathogen, PtoDC3000, and a tomato pathogen that is a nonhost on Arabidopsis,
PtoT1. By studying the conserved and variant molecular elements generally thought to define the host range
of P. syringae, such as effectors, toxins, and defense-inducing pathogen-associated molecular patterns,
between these two strains, I hope to unravel the molecular pathways that allow Arabidopsis to be resistant to
PtoT1 despite being susceptible to the closely related PtoDC3000. Additionally the Vinatzer lab has recently
sequenced several PtoT1-like strains and several PtoDC3000-like strains. Utilizing comparative genomics,
I will focus on conserved differences between these two groups as we hypothesize such differences are more likely to
define host range than genetic anomalies represented by only one or two strains.
Manuscript in press:
Submitted Manuscript:
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