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Abstract
Disease suppressive soils are soils in which plants do not get diseased from plant pathogens due to the presence (and activities) of the microbes present in the soil. Understanding which microbes contribute to confer suppression and through which mechanisms they can protect plants is crucial for a sustainable control of plant diseases. In the research conducted in this thesis, I first examined the role of Lysobacter species, previously associated with disease suppressive soils, in suppressing damping-off disease caused by the soil-borne fungal pathogen Rhizoctonia solani on sugar beet. The majority of the Lysobacter strains tested revealed a broad metabolic potential in producing a variety of enzymes and secondary metabolites able to suppress R. solani in vitro. However, any of these strains could consistently suppress damping-off disease when applied in soil bioassays. Their ability to promote plant growth was also tested for sugar beet, cauliflower, onion or Arabidopsis thaliana. Results indicated that any of the Lysobacter strains could consistently promote plant growth, neither via direct contact nor via volatile production. Second, I investigated whether the antagonistic activity of Lysobacter species could be triggered when applied as bacterial consortia, together with Pseudomonas and Streptomyces species. Although several bacterial combinations showed an increased antagonistic effect towards R. solani in vitro, no consistent effects were observed when these bacterial consortia were applied in vivo. Third, I investigated the dynamical changes in the bacterial community composition and functions occurring during the process of disease suppressiveness induction by performing whole community analyses using next-generation sequencing techniques. Results indicated that suppressiveness induction was most associated with changes in certain bacterial traits rather than changes in the bacteria community composition itself. Among the functions found as more active in suppressive soils were several ‘classic’ mechanisms of disease suppression, including competition for nutrients, iron and space and production of extracellular enzymes, indol-acetic-acid and hydrogen cyanide. Among the enzymes found in higher abundance in suppressive soil were these ones involved in the degradation of oxalic acid, a pathogenicity factor produced by pathogenic fungi to help infecting the host plant. Hence, I finally studied the role of bacteria able to produce enzymes able to degrade oxalic acid in suppressing R. solani disease. Enrichment of native oxalotrophic bacteria existing in soil, their isolation and further application into soil revealed that they could effectively suppress Rhizoctonia disease. Characterization of these oxalotrophic bacteria revealed that members within the Caulobacter and Nocardioides species could suppress R. solani disease by their own. Furthermore, the research done in this thesis highlights the importance of combining different techniques to unravel the mechanisms underlying disease suppression and the importance of studying function-over-phylogeny. Additionally, it also highlights the importance of organic amendments (such as oxalic acid) directly into soils in order to “engineer” the bacterial functions towards the control of diseases caused by R. solani.
Original language | English |
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Qualification | Doctor of Philosophy |
Awarding Institution |
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Supervisors/Advisors |
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Award date | 15 Jun 2017 |
Place of Publication | Wageningen |
Publisher | |
Print ISBNs | 9789463431774 |
DOIs | |
Publication status | Published - 15 Jun 2017 |
Keywords
- suppressive soils
- soil suppressiveness
- plant diseases
- thanatephorus cucumeris
- microbial ecology
- soil microbiology
- rhizosphere bacteria
- soil bacteria
- community ecology
- soil fungi
- transcriptomics
- taxonomy
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- 1 Finished
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Ecology and genomics of Lysobacter species: toward the development of new disease control strategies
Gomez Exposito, R. (PhD candidate), Govers, F. (Promotor), Raaijmakers, J. (Promotor) & Postma, J. (Co-promotor)
21/03/12 → 15/06/17
Project: PhD