Summary
I will use my MSCA-IF in the Stukenbrock Lab to dissect the molecular interactions between the fungal pathogen, Zymoseptoria tritici, and its host plant, wheat. Despite being the most devastating fungal wheat disease in Europe, little is known about the molecular mechanisms used by Z. tritici to cause disease. I propose to undertake a project that will use my expertise in molecular biology, combined with the Stukenbrock Lab's expertise in fungal genomics and evolution, to build a better understanding of how Z. tritici is able to evade host immune defences in order to grow, develop and, ultimately, induce disease symptoms.
Plant pathogens use secreted proteins, described as effectors, to suppress host defences and/or alter host metabolism. However, few effectors from Z. tritici have been characterised. I aim to identify effectors that are used by Z. tritici to suppress wheat immune systems. To select effector candidates, I will use the Stukenbrock Lab's Zymoseptoria genomic resources to compare the variation in effector complements among Z. tritici and its closely related sister species. Z. tritici can infect wheat and not wild grass species. Inversely, Z. tritici's sister species infect wild grasses, but cannot infect wheat. Therefore, I hypothesise that effectors shared among all of these species are candidates as suppressors of conserved plant immune systems, whereas, effectors unique to Z. tritici, and conserved among all isolates of this fungus, are likely involved in host specialisation. I will screen the former set of effector candidates for their ability to suppress BAK1-dependent immune responses (an immune pathway conserved among a divergent range of plant species). I will knock-out the genes encoding the latter set of effectors, and will screen whether the virulence of the resulting mutants is reduced. Combined, these two approaches will help assign functions to more Z. tritici effectors and, thereby, develop new insights into this devastating disease.
Plant pathogens use secreted proteins, described as effectors, to suppress host defences and/or alter host metabolism. However, few effectors from Z. tritici have been characterised. I aim to identify effectors that are used by Z. tritici to suppress wheat immune systems. To select effector candidates, I will use the Stukenbrock Lab's Zymoseptoria genomic resources to compare the variation in effector complements among Z. tritici and its closely related sister species. Z. tritici can infect wheat and not wild grass species. Inversely, Z. tritici's sister species infect wild grasses, but cannot infect wheat. Therefore, I hypothesise that effectors shared among all of these species are candidates as suppressors of conserved plant immune systems, whereas, effectors unique to Z. tritici, and conserved among all isolates of this fungus, are likely involved in host specialisation. I will screen the former set of effector candidates for their ability to suppress BAK1-dependent immune responses (an immune pathway conserved among a divergent range of plant species). I will knock-out the genes encoding the latter set of effectors, and will screen whether the virulence of the resulting mutants is reduced. Combined, these two approaches will help assign functions to more Z. tritici effectors and, thereby, develop new insights into this devastating disease.
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More information & hyperlinks
| Web resources: | https://cordis.europa.eu/project/id/101031091 |
| Start date: | 01-04-2021 |
| End date: | 31-03-2023 |
| Total budget - Public funding: | 162 806,40 Euro - 162 806,00 Euro |
Cordis data
Original description
I will use my MSCA-IF in the Stukenbrock Lab to dissect the molecular interactions between the fungal pathogen, Zymoseptoria tritici, and its host plant, wheat. Despite being the most devastating fungal wheat disease in Europe, little is known about the molecular mechanisms used by Z. tritici to cause disease. I propose to undertake a project that will use my expertise in molecular biology, combined with the Stukenbrock Lab's expertise in fungal genomics and evolution, to build a better understanding of how Z. tritici is able to evade host immune defences in order to grow, develop and, ultimately, induce disease symptoms.Plant pathogens use secreted proteins, described as effectors, to suppress host defences and/or alter host metabolism. However, few effectors from Z. tritici have been characterised. I aim to identify effectors that are used by Z. tritici to suppress wheat immune systems. To select effector candidates, I will use the Stukenbrock Lab's Zymoseptoria genomic resources to compare the variation in effector complements among Z. tritici and its closely related sister species. Z. tritici can infect wheat and not wild grass species. Inversely, Z. tritici's sister species infect wild grasses, but cannot infect wheat. Therefore, I hypothesise that effectors shared among all of these species are candidates as suppressors of conserved plant immune systems, whereas, effectors unique to Z. tritici, and conserved among all isolates of this fungus, are likely involved in host specialisation. I will screen the former set of effector candidates for their ability to suppress BAK1-dependent immune responses (an immune pathway conserved among a divergent range of plant species). I will knock-out the genes encoding the latter set of effectors, and will screen whether the virulence of the resulting mutants is reduced. Combined, these two approaches will help assign functions to more Z. tritici effectors and, thereby, develop new insights into this devastating disease.
Status
CLOSEDCall topic
MSCA-IF-2020Update Date
28-04-2024
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