Effects of viral infections on Ca2+ homeostasis in plants

Calcium ions (Ca2+) are the universal messengers that fine-tune various processes in every living cell, including antiviral responses. To date, in plants the role of Ca2+ signaling during viral infections has been studied insufficiently, particularly the molecular mechanisms of Ca2+-dependent events remain to be identified in many cases. My aim is to determine how plant viruses alter Ca2+ fluxes at different subcellular locations and to identify the key viral components, which are responsible for such changes in Ca2+ signaling. To this end, I will infect the powerful model plant Arabidopsis thaliana with RNA- and DNA-genome containing viruses. First, I will determine the stages of viral infection, at which normal Ca2+ signaling is altered, and which subcellular Ca2+ depots are targeted by the plant viruses. The next step will be to determine which viral proteins trigger Ca2+-dependent defense of the plant and which ones are able to suppress such a defense by altering certain steps of Ca2+ signaling. This project will reveal the role of Ca2+ in plant antiviral defense and elucidate the mechanisms of how viruses manipulate the host Ca2+ signaling that allows the virus to establish successful infection. Moreover, it will lay the ground for further research on this topic, which is very important, because the detailed knowledge of the Ca2+ fluxes regulation mechanisms is essential for understanding the basic antiviral defense responses and therefore would open new opportunities for crops defense in agriculture.

Calcium ions (Ca2+) serve as vital messengers that regulate numerous processes within every living cell, including antiviral responses. Presently, the understanding of Ca2+ signaling during viral infections in plants remains somewhat limited, particularly concerning the intricate molecular mechanisms underlying Ca2+-dependent events, which are yet to be identified. The primary objective of this project was to ascertain the manner in which plant viruses induce changes in Ca2+ fluxes across distinct subcellular localizations, and to pinpoint the essential viral components responsible for these alterations in Ca2+ signaling. To achieve this, the highly informative model organism, Arabidopsis thaliana, was subjected to infections with viruses containing RNA and DNA genomes. Our findings highlighted the involvement of a mitochondrial protein and two chloroplast proteins in rendering susceptibility to viral infections. This endeavor significantly enhances our comprehension of the role of Ca2+ in plant antiviral defense and elucidates the mechanisms through which viruses manipulate the host's Ca2+ signaling for establishment of a successful viral infection. This project not only advances our insights into this aspect but also paves the way for future investigations in this filed. Learning of the regulatory mechanisms governing Ca2+ fluxes is pivotal for comprehending fundamental antiviral defense responses. Consequently, it opens up novel avenues for bolstering agricultural defenses in crops.