Investigating the role of S-nitrosylation in plant antiviral defense
Item statusRestricted Access
Embargo end date31/07/2022
S-Nitrosylation, a post-translational modification, involves specific reversible incorporation of nitric oxide (NO) moiety to protein cysteine thiol to form an S-nitrosothiol (SNO). The cellular level of S-nitrosylation is maintained by S-nitroso glutathione reductase (GSNOR), an enzyme involved in the turnover of NO reservoir, S-nitroso glutathione (GSNO). Loss of function of AtGSNOR1 leads to increased SNO level and compromised immune response against bacterial and fungal pathogens. Similar consequences are observed in plants with excessive NO production. However, not much is known about the role of S-nitrosylation in antiviral response in plants which we aim to tackle in this study. Arabidopsis mutants with varying level of nitric oxide (NO) and SNO: gsnor1-3, gsnor1-3R, nox1, TRXh5 (nox1) were selected. These mutants along with controls (Col-0, eIF(iso)4E‐1) were inoculated with a Green Fluorescent Protein (GFP)-tagged potyvirus, Turnip mosaic virus (TuMV-GFP) to study susceptibility to viral infection. The susceptibility assay demonstrated higher viral resistance in plants with increased SNO levels. This observation contrasts with the observation made with bacterial and fungal pathogens. Multiple facets associated with both host and pathogen were explored, to understand the underlying mechanism behind TuMV resistance in plants with higher SNO level. To achieve this, we focused on gsnor1-3 mutants due to clearly displayed delayed viral infection, infection progression pattern and ease of viral inoculation. This SNO mutant displayed slower onset of viral infection in rub-inoculated leaves, however viral replication rate and cell to cell movement was not hampered. We found that the systemic movement of TuMV was slower and delayed in gsnor1-3 plants. This was confirmed by evaluation of gsnor1-3 morphology that showed variation in plasmodesmata number, vascular pattern, and phloem transport rate, suggesting cumulative effect of host factors on delayed viral movement.