Editing strigolactone hormone receptor for robust antiviral silencing in rice
Summary
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 recept
Content
# Editing strigolactone hormone receptor for robust antiviral silencing in rice
*Published: 2026 Apr 2*
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.
DOI: 10.1016/j.cell.2026.01.013