# Transcriptional and hormonal profiling uncovers the interactions between plant developmental stages and RNA virus infection

## TL;DR

This study shows that Arabidopsis plants infected at later developmental stages are more susceptible to viruses but also more fertile, suggesting a trade-off between infection resistance and plant reproduction.

## Contribution

The study reveals a development-dependent trade-off between viral susceptibility and fertility in Arabidopsis.

## Key findings

- Infected mature flowering plants are more fertile than those infected at earlier stages.
- Salicylic acid treatment increases resistance to infection but reduces fertility in mature plants.
- Downregulation of cell wall biosynthetic genes in later stages may facilitate viral spread.

## Abstract

Arabidopsis thaliana is more susceptible to certain viruses during its later developmental stages. The differential responses and the mechanisms behind this development-dependent susceptibility to infection are still not fully understood. Here we explored the outcome of a viral infection at different host developmental stages by studying the response of A. thaliana to infection with turnip mosaic virus at three developmental stages: juvenile vegetative, bolting, and mature flowering plants. We found that infected plants at later stages downregulate cell wall biosynthetic genes and that this downregulation may be one factor facilitating viral spread and systemic infection. We also found that, despite being more susceptible to infection, infected mature flowering plants were more fertile (i.e. produce more viable seeds) than juvenile vegetative and bolting infected plants; that is, plants infected at the reproductive stage have greater fitness than plants infected at earlier developmental stages. Moreover, treatment of mature plants with salicylic acid increased resistance to infection at the cost of significantly reducing fertility. Together, these observations support a negative trade-off between viral susceptibility and plant fertility. Our findings point towards a development-dependent tolerance to infection.