Suppression of a dsRNA-induced plant immunity pathway by viral movement protein

Abstract

SummaryThe virome of plants is dominated by RNA viruses 1 and several of these cause devastating diseases in cultivated plants leading to global crop losses 2. To infect plants, RNA viruses engage in complex interactions with compatible plant hosts. In cells at the spreading infection front, RNA viruses replicate their genome through double-stranded RNA (dsRNA) intermediates and interact with cellular transport processes to achieve cell-to-cell movement of replicated genome copies through cell wall channels called plasmodesmata (PD) 3. In order to propagate, viruses also must overcome host defense responses. In addition to triggering the antiviral RNA silencing response, RNA virus infection also elicits pattern-triggered immunity (PTI) 4 whereby dsRNA, a hallmark of virus replication, acts as an important elicitor 5. This innate antiviral immune response is also triggered when dsRNA is applied externally and does not require sequence homology to the virus 5. However, the mechanism by which PTI restricts virus infection is not known. Here, we show that dsRNA inhibits the progression of virus infection by triggering callose deposition at plasmodesmata and the inhibition of transport through these cell-to-cell communication channels. The dsRNA-induced signaling pathway leading to callose deposition is independent of ROS production and thus distinguished from pathways triggered by bacterial and fungal elicitors. The dsRNA-induced host response at plasmodesmata is suppressed by the Tobacco mosaic virus movement protein (MP). Thus, the virus uses MP to inhibit innate dsRNA-induced immunity at plasmodesmata, which could be a general strategy of phytoviruses to overcome plant defenses and spread infection.

Extracellular Self- and Non-Self DNA Involved in Damage Recognition in the Mistletoe Parasitism of Mesquite Trees

“…We observed a pattern of SA contents in both self and non-self exDNA treatments, with high amounts at early and late times. In that aspect, many authors have reported that SA peaked minutes after or at 24 h after DAMP sources, similar to our results reported here [ 25 , 32 , 36 , 55 , 57 , 87 ]. Notably, we detected an increase in ABA contents with non-self exDNA treatment at 2 h after treatment.…”

“…Under mechanical damage and after applying 100 µg/mL of self-exDNA, we found a rise in JA levels associated with an oxidative burst; however, non-self exDNA treatment did not affect JA levels. Additionally, JA levels were found with the application of exDNA sources in a similar way to the different reports mentioned [ 25 , 32 , 36 , 55 , 57 , 87 ]. Additionally, we quantified SA and ABA, and four canonical growth regulatory hormones such as Zeatin, Kinetin, iP, and IAA derived from the self and non-self exDNA applications.…”

“…These molecules function outside of the cell as elicitors, triggering reactions that promote tissue repair and immunization in order to prevent potential infections [ 24 ]. Additionally, plants can detect peptidoglycans or chitin to distinguish between self and nonself fragments of the cell wall [ 20 ], self RNA from double-stranded RNA [ 25 ], and self-DNA from microbial DNA by perception of GC-rich islands in unmethylated CpG motifs [ 26 , 27 ]. Nevertheless, in the case of mistletoe parasitism, the host plant must distinguish its self-patterns from those of the other plant.…”