Dokument: The infection biology of the smut fungus Thecaphora thlaspeos and its molecular cross-talk with its Brassicaceae hosts
Titel: | The infection biology of the smut fungus Thecaphora thlaspeos and its molecular cross-talk with its Brassicaceae hosts | |||||||
URL für Lesezeichen: | https://docserv.uni-duesseldorf.de/servlets/DocumentServlet?id=45273 | |||||||
URN (NBN): | urn:nbn:de:hbz:061-20180327-095739-0 | |||||||
Kollektion: | Dissertationen | |||||||
Sprache: | Englisch | |||||||
Dokumententyp: | Wissenschaftliche Abschlussarbeiten » Dissertation | |||||||
Medientyp: | Text | |||||||
Autor: | Courville, Kaitlyn [Autor] | |||||||
Dateien: |
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Beitragende: | Prof. Dr. Feldbrügge, Michael [Gutachter] Prof. Dr. Rose, Laura [Gutachter] | |||||||
Dewey Dezimal-Klassifikation: | 500 Naturwissenschaften und Mathematik » 570 Biowissenschaften; Biologie | |||||||
Beschreibung: | Modern agriculture faces challenges to increase overall crop yield in order to feed a growing population. A key factor contributing to these challenges include the impact of biotic stress on crops, of which fungal pathogens instigate a large portion and are therefore crucial to study in order to develop agricultural practices that can mitigate their impact. A prominent order of plant pathogenic fungi within the Basidiomycete phylum is the Ustilaginales, commonly known as “smut fungi”, which mostly infect grasses. Despite the vast information and tools that exist to functionally study the model smut fungus that infects maize, Ustilago maydis, especially regarding pathogenicity, the genetics of its maize host remain complex. To date, an R-gene that confers resistance to U. maydis remains to be identified, cloned, and ultimately introduced into maize. Furthermore, the genetic complexity of the host has also made it difficult to functionally characterize host responses to smut fungal infection. Thecaphora thlaspeos is the only described smut fungus to infect within the Brassicaceae family. Here, I present the infection process of T. thlaspeos, whose spores I have collected annually in the field, which displayed that germ tubes arising from germinating spores can directly enter the roots and leaves of the host. T. thlaspeos eventually proliferates throughout the entire plant in an endophyte-like fashion and infection studies showed that T. thlaspeos infects several Arabis spps. as well as the model plant Arabidopsis thaliana. Extensive confocal microscopy indicated that T. thlaspeos colonization occurs along but outside the host vasculature tissues, contrary to other systemic-infecting smut fungi. The establishment of this infection system in the lab successfully led to the sporulation of T. thlaspeos in silique tissue of Ar. hirsuta, these host plants otherwise lacking obvious infection symptoms. Transcriptome analysis on T. thlaspeos-infected Ar. hirsuta revealed that in planta induced fungal genes are enriched for unique, secreted proteins, from which I demonstrated that two have virulence functions in A. thaliana, TtNlp1 potentially suppressing PTI and TtTue1 potentially activating host immune responses. Typical for biotroph infection, my data strongly suggest that biotic stress is enriched during T. thlaspeos infection. Interestingly, the expression of several key genes involved in salicylic acid-dependent defense signaling is not significantly altered while a key gene involved in ethylene-dependant defense signaling is induced, potentially indicating how T. thlaspeos behaves as a “minor” pathogen. This work lays the foundation for studying how T. thlaspeos-specific effectors likely play a role in the overall endophytic nature of this fungal pathogen and ultimately provides a more genetically accessible platform for the identification and functional characterization of R-genes that confer resistance to smut fungal pathogens. | |||||||
Lizenz: | Urheberrechtsschutz | |||||||
Fachbereich / Einrichtung: | Mathematisch- Naturwissenschaftliche Fakultät » WE Biologie » Mikrobiologie | |||||||
Dokument erstellt am: | 27.03.2018 | |||||||
Dateien geändert am: | 27.03.2018 | |||||||
Promotionsantrag am: | 20.02.2018 | |||||||
Datum der Promotion: | 15.03.2018 |