William Truman "Understanding the role of chitin related defence responses during Plasmodiophora brassicae infection" OPUS 2016-2019

Plants lack an adaptive immune response and must rely on innate recognition of pathogen markers in order to counter infections. The cell walls of microbial pathogens are one source of conserved molecular motifs that plants can identify; short chains of chitin from the walls of fungi being one such elicitor. Some protists lack chitin in their cell walls but resting spores of Plasmodiophora brassicae, the causal agent of clubroot disease in brassicas, contain 25% chitin. During the infection of Arabidopsis by P. brassicae many defence genes known to be induced by chitin are significantly suppressed, including the chitin receptor and associated signalling components. Our conjecture is that this suppression of chitin-associated signalling pathways is a critical aspect of P. brassicae virulence. The genome of P. brassicae encodes several putative secreted, chitin binding proteins; some may act to deacetylate chitin forming chitosan, a less potent elicitor of host defences, while others have no clear molecular function. Chitin-binding virulence factors in other plant pathogens can both disguise chitin from host detection and protect against hydrolysis by plant chitinases. We hypothesise that chitin binding proteins within the P. brassicae secretome contribute to the defeat of host surveillance mechanisms and the establishment of clubroot disease in Arabidopsis. Chitinase enzymes are produced by plants in response to infection; they can attack pathogens by degrading cell walls, releasing chitin oligomers that stimulate host chitin receptors and amplify danger signals. The aim of this project is to characterise the dynamics of surveillance and counter-surveillance, measures and counter-measures that pivot around this fundamental microbial structural component.

The main objectives of the project are:

  1. Characterising the cellular events involved in host chitin perception during clubroot infection of Arabidopsis and determining the contribution of chitin signalling pathways to resistance.
  2. Profiling Arabidopsis chitinase activity in response to P. brassicae and assessing clubroot pathogenicity in lines with altered chitinase activity.
  3. To survey the natural variation arising in different Arabidopsis accessions and P. brassicae pathotypes with regards to chitin signalling responses and chitinase activity during infection.
  4. Understanding the functions of P. brassicae chitin binding proteins and establishing whether they are implicated in pathogen virulence.