HEIndividual fellowship2023–2025

MAVS in plants · Mitochondrial antiviral signaling in Plants

Horizon Europe — Marie Skłodowska-Curie Actions

Duration
2023-05-01 → 2025-04-30
EU contribution
€206,888
Participants
1
Scheme
HORIZON-TMA-MSCA-PF-EF

Lines connect the coordinator with its partners.

Results in brief

Mitochondrial antiviral signaling in Plants

The systemic infections of agronomically important plants by viruses lead to significant economic losses in yield and quality of the crops. These losses are attributed to virus-induced developmental changes in the host plant, exhibited as disease symptoms. This argues for enhancing basic research to better understand and exploit the molecular mechanisms that underpin virus interference with plant development and disease resistance. Rhizomania is one of the most economically devastating disease of sugar beet and is caused by Beet necrotic yellow vein virus (BNYVV). BNYVV is a soil-borne virus transmitted by Polymyxa betae. 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. Although, progress is being made in studies of the mitochondrial signaling in response to abiotic stress and bacterial/fungal pathogen, nothing is known about how plant viruses interfere with mitochondrial signaling. 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. 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. The study has been divided into following three objectives formulated as research questions (Objective1) how BNYVV is perceived by mitochondria, (Objective 2) how mitochondria transduce signal i.e. by production of ROS, which are produced as a result of broken electron transfer chain (ETC) and (Objective 3) does mitochondrial retrograde regulation imparts resistance to virus. The advanced knowledge on the mitochondrial antiviral signaling will have implications for the wider area of virus research and, in the long run, will provide new opportunities for improvement of plant fitness and immunity in agronomic applications.

Data: CORDIS, © European Union

Project objective

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 hosts 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.

Original text from CORDIS.

Participants

  • SVERIGES LANTBRUKSUNIVERSITET · UppsalaCoordinatorSweden

Links

Data: CORDIS, © European Union