The increasing pace of global warming and climate instability will challenge the management of pests and diseases of cultivated plants. Several reports have shown that increases in environmental temperature can enhance the cell-to-cell and systemic propagation of viruses within their infected hosts. These observations suggest that earlier and longer periods of warmer weather may cause important changes in the interaction between viruses and their host’s plants, thus posing risks of new viral diseases and outbreaks in agriculture and the wild. As viruses target plasmodesmata (PD) for cell-to-cell spread, these cell wall pores may play yet unknown roles in the temperature-sensitive regulation of intercellular communication and virus infection. Understanding the temperature-sensitive mechanisms in plant-virus interactions will provide important knowledge for protecting crops against diseases in a warmer climate.

Emerging evidence indicates that in addition to its well-recognized functions in antiviral RNA silencing, dsRNA elicits pattern-triggered immunity (PTI), likely contributing to plant resistance against virus infections. However, compared to bacterial and fungal elicitor-mediated PTI, the mode-of-action and signaling pathway of dsRNA-induced defense remain poorly characterized. Here, using multi-color in vivo imaging, analysis of green fluorescent protein (GFP) mobility, callose staining and plasmodesmal marker lines in Arabidopsis thaliana and Nicotiana benthamiana, we show that dsRNA-induced PTI restricts the progression of virus infection by triggering callose deposition at plasmodesmata, thereby likely limiting the macromolecular transport through these cell-to-cell communication channels. The plasma membrane-resident SOMATIC EMBRYOGENESIS RECEPTOR-LIKE KINASE 1 (SERK1) the BOTRYTIS INDUCED KINASE1 (BIK1)/AVRPPHB SUSCEPTIBLE1 (PBS1)-LIKE KINASE1 (BIK1/PBL1) kinase module, PLASMODESMATA-LOCATED PROTEINs (PDLPs)1/2/3, as well as CALMODULIN-LIKE 41 (CML41) and Ca2+ signals are involved in the dsRNA-induced signaling leading to callose deposition at plasmodesmata and antiviral defense. Unlike the classical bacterial elicitor flagellin, dsRNA does not trigger detectable reactive oxygen species (ROS) burst, substantiating the idea that different microbial patterns trigger partially shared immune signaling frameworks with distinct features. Likely as a counter strategy, viral movement proteins from different viruses suppress the dsRNA-induced host response leading to callose deposition to achieve infection. Thus, our data support a model in which plant immune signaling constrains virus movement by inducing callose deposition at plasmodesmata and reveals how viruses counteract this layer of immunity.

Emerging evidence indicates that in addition to the well-recognized antiviral RNA silencing, dsRNA elicits responses of pattern-triggered immunity (PTI), likely contributing plant resistance against virus infections. However, compared to bacterial and fungal elicitor-mediated PTI, the mode-of-action and signaling pathway of dsRNA-induced defense remain poorly characterized. Here, using multi-color in vivo imaging by GFP mobility, staining of callose and plasmodesmal marker lines, we show that dsRNA-induced PTI restricts the progression of virus infection by triggering callose deposition at plasmodesmata, thereby likely limiting the macromolecular transport through these cell-to-cell communication channels. The plasma membrane-resident kinase module of SERK1 and BIK1/PBL1, plasmodesmata-localized proteins PDLP1/2/3 and calmodulin-like CML41, and Ca2+ signals are involved in the dsRNA-induced signaling leading to callose deposition at plasmodesmata and antiviral defense. In addition, unlike classical bacterial elicitor flagellin, dsRNA does not trigger detectable reactive oxygen species (ROS) burst, further substantiating a partially shared immune signaling framework with distinct features triggered by different microbial patterns. Likely as a counteract strategy, viral movement proteins from different viruses suppress the dsRNA-induced host response leading to callose deposition to achieve infection. Thus, our data support the new model of how plant immune signaling constrains the virus movement by inducing callose deposition at plasmodesmata and how viruses counteract this layer of immunity.