CellFeb 26, 2026

Changing a plant hormone receptor to improve antiviral defense in rice

CRISPR Gene Editing Weekly Brief ↗PubMed ↗DOI ↗

Updated Jun 27, 2026

Abstract

Essence

Editing DWARF14 at D102 let rice preserve strigolactone-dependent antiviral silencing and resist rice grassy stunt virus.

Evidence

This was a plant molecular and genome-editing study using rice, P3-DWARF14 structural and functional analyses, and cytosine base editing of two cultivars to test RGSV resistance.

Caveat

The evidence is limited to RGSV and two edited rice cultivars, so durability, field performance, and breadth against other viruses remain untested.

Simplified

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.