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The leafy gall syndrome : more than just cytokinins!

Elisabeth Stes (UGent)
(2011)
Author
Promoter
(UGent) and (UGent)
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Abstract
Rhodococcus fascians is a well-adapted soil bacterium that interacts with many plants species. Infection leads to the induction of multiple stunted shoots, resulting in the typical leafy galls. As its virulence is strictly dependent on its capacity to produce cytokinins, and the abundant shoot proliferation is a typical cytokinin effect, research on R. fascians has mainly focused on the role of these phytohormones (reviewed in Stes et al., 2011b). Intriguingly, only low levels of cytokinins are measured both in bacterial cultures and symptomatic plants (Pertry et al., 2009). Moreover, leafy gall tissue contains elevated levels of the polyamine putrescine (Depuydt et al., 2009b) and of auxin, a plant hormone known to be produced by R. fascians (Vandeputte et al., 2005). Here, we set out to investigate whether leafy gall formation is really only about cytokinins. We wondered if maybe bacterial signals could trigger a response in the plant that would reinforce or complement the action of the cytokinins and that, in the end, even would become self-sustaining. So, we analyzed the role of putrescine and auxin during the pathology (Chapter 5 and 6) and questioned if they were circumstantial by-products of the induced meristematic gall tissue or if they had an essential function and contributed to symptom formation. Important issues were to determine whether the accumulating putrescine and auxin in symptomatic tissues of Arabidopsis were of bacterial or plant origin and to establish the kinetics of these growth regulators during the course of the interaction. To get insight into the mode of action of these signaling molecules we opted to investigate the plant’s molecular response in detail by profiling the expression of genes implicated in the biosynthesis and signal transduction of these phytohormones and of marker genes for symptom development during leafy gall formation. Analysis of the response of selected Arabidopsis mutants and complementary pharmacological approaches had to provide additional data to allow the extension of the model on the molecular basis of the leafy gall syndrome (Depuydt, 2009). The very broad host range of R. fascians implies that it can efficiently suppress or circumvent the defense systems of an extensive variety of plants, but the question as to which strategy the pathogen employs to do so remained open. Possibly, R. fascians is not recognized as a pathogen by the host or alternatively, it modulates the plant’s auxin metabolism to repress defense responses as reported for other plant microbial pathosystems (Kazan and Manners, 2010). To unravel the relevance of plant defense reactions during the R. fascians – Arabidopsis interaction, we chose to evaluate transcriptional and metabolic modulations related to basal host defenses upon R. fascians infection. Infecting mutants impaired in specific defense pathways had to substantiate our findings and permit for the first time to document on how a broad-spectrum Gram-positive phytopathogen deals with plant defense (Chapter 7). Altogether, with these experimental approaches we aim at expanding the understanding on the pathogenic strategies of R. fascians and on the molecular cross-talk between R. fascians and Arabidopsis that ultimately lead to the formation of a leafy gall. However, we also hope that our results support our point of view that the R. fascians-induced pathology is a valuable model system to study regular plant development.

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Citation

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MLA
Stes, Elisabeth. The Leafy Gall Syndrome : More than Just Cytokinins! Ghent University. Faculty of Sciences, 2011.
APA
Stes, E. (2011). The leafy gall syndrome : more than just cytokinins! Ghent University. Faculty of Sciences, Ghent, Belgium.
Chicago author-date
Stes, Elisabeth. 2011. “The Leafy Gall Syndrome : More than Just Cytokinins!” Ghent, Belgium: Ghent University. Faculty of Sciences.
Chicago author-date (all authors)
Stes, Elisabeth. 2011. “The Leafy Gall Syndrome : More than Just Cytokinins!” Ghent, Belgium: Ghent University. Faculty of Sciences.
Vancouver
1.
Stes E. The leafy gall syndrome : more than just cytokinins! [Ghent, Belgium]: Ghent University. Faculty of Sciences; 2011.
IEEE
[1]
E. Stes, “The leafy gall syndrome : more than just cytokinins!,” Ghent University. Faculty of Sciences, Ghent, Belgium, 2011.
@phdthesis{3006324,
  abstract     = {{Rhodococcus fascians is a well-adapted soil bacterium that interacts with many plants species. Infection leads to the induction of multiple stunted shoots, resulting in the typical leafy galls. As its virulence is strictly dependent on its capacity to produce cytokinins, and the abundant shoot proliferation is a typical cytokinin effect, research on R. fascians has mainly focused on the role of these phytohormones (reviewed in Stes et al., 2011b). Intriguingly, only low levels of cytokinins are measured both in bacterial cultures and symptomatic plants (Pertry et al., 2009). Moreover, leafy gall tissue contains elevated levels of the polyamine putrescine (Depuydt et al., 2009b) and of auxin, a plant hormone known to be produced by R. fascians (Vandeputte et al., 2005). Here, we set out to investigate whether leafy gall formation is really only about cytokinins. We wondered if maybe bacterial signals could trigger a response in the plant that would reinforce or complement the action of the cytokinins and that, in the end, even would become self-sustaining. So, we analyzed the role of putrescine and auxin during the pathology (Chapter 5 and 6) and questioned if they were circumstantial by-products of the induced meristematic gall tissue or if they had an essential function and contributed to symptom formation. Important issues were to determine whether the accumulating putrescine and auxin in symptomatic tissues of Arabidopsis were of bacterial or plant origin and to establish the kinetics of these growth regulators during the course of the interaction. To get insight into the mode of action of these signaling molecules we opted to investigate the plant’s molecular response in detail by profiling the expression of genes implicated in the biosynthesis and signal transduction of these phytohormones and of marker genes for symptom development during leafy gall formation. Analysis of the response of selected Arabidopsis mutants and complementary pharmacological approaches had to provide additional data to allow the extension of the model on the molecular basis of the leafy gall syndrome (Depuydt, 2009). The very broad host range of R. fascians implies that it can efficiently suppress or circumvent the defense systems of an extensive variety of plants, but the question as to which strategy the pathogen employs to do so remained open. Possibly, R. fascians is not recognized as a pathogen by the host or alternatively, it modulates the plant’s auxin metabolism to repress defense responses as reported for other plant microbial pathosystems (Kazan and Manners, 2010). To unravel the relevance of plant defense reactions during the R. fascians – Arabidopsis interaction, we chose to evaluate transcriptional and metabolic modulations related to basal host defenses upon R. fascians infection. Infecting mutants impaired in specific defense pathways had to substantiate our findings and permit for the first time to document on how a broad-spectrum Gram-positive phytopathogen deals with plant defense (Chapter 7). Altogether, with these experimental approaches we aim at expanding the understanding on the pathogenic strategies of R. fascians and on the molecular cross-talk between R. fascians and Arabidopsis that ultimately lead to the formation of a leafy gall. However, we also hope that our results support our point of view that the R. fascians-induced pathology is a valuable model system to study regular plant development.}},
  author       = {{Stes, Elisabeth}},
  language     = {{eng}},
  pages        = {{223 + annexes}},
  publisher    = {{Ghent University. Faculty of Sciences}},
  school       = {{Ghent University}},
  title        = {{The leafy gall syndrome : more than just cytokinins!}},
  year         = {{2011}},
}