Areca palm velarivirus 1 encoded CP suppresses antiviral RNA silencing by mediating the autophagic degradation of SGS3 and disrupting the SGS3–RDR6 interaction

TL;DR

This study reveals how a virus in areca palms evades the plant's antiviral defenses by degrading a key protein and disrupting its interactions.

Contribution

The study identifies a novel dual mechanism by which APV1 CP suppresses RNA silencing through autophagic degradation and complex disruption.

Findings

APV1 CP acts as a viral suppressor of RNA silencing by inhibiting local and systemic silencing.

CP promotes the autophagic degradation of AcSGS3, a key RNA silencing component.

CP disrupts the interaction between SGS3 and AcRDR6, impairing RNAi signaling.

Abstract

Areca palm velarivirus 1 (APV1) is the causative agent of yellow leaf disease (YLD), leading to severe yield losses in areca palms. However, how APV1 counteracts host immunity remains largely underexplored, and the underlying mechanisms are still poorly understood. RNA silencing is an evolutionarily conserved antiviral defense mechanism in eukaryotes. In this study, we identify the APV1-encoded capsid protein (CP) as a viral suppressor of RNA silencing (VSR) that inhibits both local and systemic silencing triggered by single-stranded RNA (ssRNA). Mechanistically, CP interacts with host Suppressor of Gene Silencing 3 (AcSGS3), a key component of the RNA silencing pathway, and promotes its degradation via autophagy. Additionally, CP disrupts the SGS3–AcRDR6 (RNA-dependent RNA polymerase 6) interaction, impairing the RNAi signaling cascade. Our findings reveal a novel dual mechanism to counteract host RNA silencing in which APV1 CP disrupts the SGS3–AcRDR6 complex and exploits the autophagic pathway to degrade AcSGS3, thereby undermining host antiviral defenses.

The online version contains supplementary material available at 10.1007/s44154-025-00279-w.

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