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

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Publisher

MDPI
DOI: 10.3390/ijms241713625

Keywords

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

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Virus-specific proteins can trigger hypersensitive response (HR) in plants, which is a type of cell death. The main cell death signaling pathway involves the interaction between HR-inducing proteins and nucleotide-binding leucine-rich repeats (NLR) proteins encoded by plant resistance genes. NLR proteins can act as both sensors and helpers, or form an activation network leading to oligomerization and formation of membrane-associated resistosomes.
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.

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