Signaling and Resistosome Formation in Plant Innate Immunity to Viruses: Is There a Common Mechanism of Antiviral Resistance Conserved across Kingdoms?

Abstract

Virus-specific proteins, including coat proteins, movement proteins, replication proteins, and suppressors of RNA interference are capable of triggering the hypersensitive response (HR), which is a type of cell death in plants. The main cell death signaling pathway involves direct interaction of HR-inducing proteins with nucleotide-binding leucine-rich repeats (NLR) proteins encoded by plant resistance genes. Singleton NLR proteins act as both sensor and helper. In other cases, NLR proteins form an activation network leading to their oligomerization and formation of membrane-associated resistosomes, similar to metazoan inflammasomes and apoptosomes. In resistosomes, coiled-coil domains of NLR proteins form Ca²⁺ channels, while toll-like/interleukin-1 receptor-type (TIR) domains form oligomers that display NAD+ glycohydrolase (NADase) activity. This review is intended to highlight the current knowledge on plant innate antiviral defense signaling pathways in an attempt to define common features of antiviral resistance across the kingdoms of life.

Keywords: hypersensitive response; nucleotide-binding leucine-rich proteins; plant virus; programmed cell death; resistosome.

Figure 1

Schematic representation of plant NLR signaling and resistosome formation alongside the animal apoptosome and inflammasome, and the main programmed cell death (PCD) pathways. (A) Plant signaling network. CNL, RNL, TNL pathways are shown in blue, pale blue, and green, respectively. Avr effectors are displayed in orange and helper lipases are displayed in yellow. (B) Animal apoptosome (APAF-1) and inflammasome (NAIP2/NLRC4) are shown in red. (C) Chimeric “plant inflammasome” generated with fusion protein consisting of plant TIR domain and animal NLRC4 subunit is shown in purple. Dotted lines demonstrate the intended pathways.