Editing strigolactone hormone receptor for robust antiviral silencing in rice

Feb 26, 2026Cell

Changing a plant hormone receptor to improve antiviral defense in rice

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CRISPR Gene Editing on OpenScience ↗PubMed ↗DOI ↗

Abstract

A single D102N substitution in the DWARF14 receptor can confer resistance to rice grassy stunt virus (RGSV).

Strigolactone hormone signaling enhances antiviral defenses in rice by activating RNA-dependent RNA polymerases RDR1 and RDR6.
The protein P3 of RGSV inhibits strigolactone signaling by binding to and sequestering the receptor DWARF14.
The D102 residue in DWARF14 is critical for its interaction with P3 but does not affect strigolactone perception.
Editing DWARF14 to introduce the D102N substitution can prevent RGSV from suppressing antiviral defenses.

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The small interfering RNA (siRNA) pathway directs broad-spectrum antiviral defense through RNA silencing so that virulent infection requires efficient suppression of the defense mechanism. Here, we show that strigolactone (SL) hormone signaling promotes antiviral silencing in rice plants by transcriptional activation of RNA-dependent RNA polymerase 1 (RDR1) and RDR6. We demonstrate that protein P3 of the rice grassy stunt virus (RGSV) blocks SL signaling by directly sequestering the receptor DWARF14 from DWARF3. Structural and functional analyses of the P3-DWARF14 complex reveal that the aspartic acid at position 102 (D102) of DWARF14 is essential for the P3 interaction but not for SL perception. Notably, a single D102N substitution of DWARF14, introduced into two rice cultivars by cytosine base editing (CBE) confers resistance against RGSV by blocking viral suppression of SL signaling-dependent antiviral silencing. Our findings establish a transgene-free strategy for engineering disease resistance by precise genome editing of the SL receptor to escape pathogen suppression of the endogenous defense pathway.