Summary
Rhizomania is one of the most economically devastating disease of sugar beet and is caused by Beet necrotic yellow vein virus (BNYVV). Emerging evidence indicates that mitochondria plays essential role in plant immunity and thus represents a promising target for the development of sustainable broad-spectrum disease resistance in crops. This project builds on the previous findings that BNYVV localize to mitochondria, and this occurrence is related to the assembly of the virus. Moreover, several nuclear genes encoding mitochondrial proteins appear to be repressed by a nuclear-localized BNYVV P25 virulence factor (Savenkov, unpublished). In animals, mitochondrial signaling in response to virus infection has been well studied, but it has been overlooked in plants and still is an open field to find the potential targets for improved plant fitness against plant viruses. Mitochondria activate antiviral signaling in response to virus infection in animals, but so far no such mechanism is known in plants. The mitochondria exert its response via nucleus by a process called mitochondrial retrograde regulation (MRR). Mitochondrial homeostasis translates pathogen infection into molecular mechanisms associated with chromatin remodeling thereby conferring resistance to pathogens. Mitochondria remodel chromatin structure via MRR and activate defense related genes to fight off the pathogen. The rationale behind this proposal is discoveries from the host’s group showing that promoter elements of mitochondrial genes (Tim13, Cyt c) are the targets of p25 protein of BNYVV (as was identified by ChIP-seq; unpublished data). This project has the overarching aim to deepen our understanding of the mitochondrial events underlying antiviral response, with the long-term goal to provide knowledge-based tools for improved plant performance under pathogen attack.
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| Web resources: | https://cordis.europa.eu/project/id/101110045 |
| Start date: | 01-05-2023 |
| End date: | 30-04-2025 |
| Total budget - Public funding: | - 206 887,00 Euro |
Cordis data
Original description
Rhizomania is one of the most economically devastating disease of sugar beet and is caused by Beet necrotic yellow vein virus (BNYVV). Emerging evidence indicates that mitochondria plays essential role in plant immunity and thus represents a promising target for the development of sustainable broad-spectrum disease resistance in crops. This project builds on the previous findings that BNYVV localize to mitochondria, and this occurrence is related to the assembly of the virus. Moreover, several nuclear genes encoding mitochondrial proteins appear to be repressed by a nuclear-localized BNYVV P25 virulence factor (Savenkov, unpublished). In animals, mitochondrial signaling in response to virus infection has been well studied, but it has been overlooked in plants and still is an open field to find the potential targets for improved plant fitness against plant viruses. Mitochondria activate antiviral signaling in response to virus infection in animals, but so far no such mechanism is known in plants. The mitochondria exert its response via nucleus by a process called mitochondrial retrograde regulation (MRR). Mitochondrial homeostasis translates pathogen infection into molecular mechanisms associated with chromatin remodeling thereby conferring resistance to pathogens. Mitochondria remodel chromatin structure via MRR and activate defense related genes to fight off the pathogen. The rationale behind this proposal is discoveries from the host’s group showing that promoter elements of mitochondrial genes (Tim13, Cyt c) are the targets of p25 protein of BNYVV (as was identified by ChIP-seq; unpublished data). This project has the overarching aim to deepen our understanding of the mitochondrial events underlying antiviral response, with the long-term goal to provide knowledge-based tools for improved plant performance under pathogen attack.Status
SIGNEDCall topic
HORIZON-MSCA-2022-PF-01-01Update Date
31-07-2023
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