A viral strategy to hijack the miR156–SPL–ICS1 module suppresses salicylic acid‐based immunity in rice

Feb 9, 2026Journal of integrative plant biology

A virus uses a small RNA system to weaken rice’s salicylic acid immune response

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Abstract

Rice grassy stunt virus (RGSV) suppresses antiviral immunity by targeting the miR156-SPL-ICS1 module.

RGSV P3 binds to a specific sequence in the miR156a promoter, leading to increased levels of miR156.
Elevated miR156 levels repress the expression of SPL14 and SPL17, which are involved in salicylic acid biosynthesis.
Infection with RGSV is linked to decreased protein levels of SPL14 and SPL17.
Loss of SPL14 or SPL17 function results in reduced salicylic acid accumulation and weakened antiviral defense.
Overexpression of SPL14 or SPL17 can alleviate RGSV symptoms and limit viral replication.
Exogenous salicylic acid can restore immune responses and improve growth defects associated with RGSV infection.

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Plant viruses frequently reprogram conserved growth-defense regulatory hubs to promote infection. Here, we show that the rice grassy stunt virus (RGSV) suppresses salicylic acid (SA)-mediated antiviral immunity by targeting the miR156-SPL-ICS1 module. The viral effector P3 directly binds a conserved 12-bp cis-element in the miR156a promoter, activating its transcription and increasing miR156 accumulation. Increased miR156 represses SPL14 and SPL17 transcripts, while RGSV infection is also associated with a pronounced reduction in SPL14/17 protein abundance. P3 physically associates with SPL14 and SPL17, indicating an additional post-transcriptional layer contributing to SPL attenuation. Genetic analyses demonstrate that SPL14 and SPL17 positively regulate ICS1, a key enzyme in SA biosynthesis, and that loss of SPL14/17 function compromises SA accumulation and antiviral defense. Conversely, overexpression of SPL14 or SPL17 mitigates RGSV symptoms and restricts viral accumulation, whereas exogenous SA restores immunity and partially rescues disease-associated architectural defects. Together, our findings reveal a dual-layer virulence strategy in which RGSV P3 coordinately suppresses the miR156-SPL14/17-ICS1 pathway at transcriptional and post-transcriptional levels, uncovering a central regulatory node that links rice development and antiviral immunity and providing actionable targets for engineering RGSV-resistant rice.

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A viral strategy to hijack the miR156–SPL–ICS1 module suppresses salicylic acid‐based immunity in rice

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