Light induces Phytochrome B SUMOylation to recruit the immune regulator NPR1 in nuclear condensates to control immunity in plants

It has long been observed that light perception by phytochromes control plant immunity, however, the underpinning molecular mechanism is less well understood. We demonstrate that light mediated SUMO conjugation to Phytochrome B (PhyB) is critical for increasing cellular salicylic-acid (SA) levels to orchestrate systemic acquired resistance (SAR) upon avirulent bacterial infection. SUMOylation is critical for PhyB nuclear condensate formation during light activated immunity. Light induced PhyB SUMOylation recruits NPR1, through its SUMO interacting motif to nuclear condensates to elevate SA levels for immune responses. In the dark during SAR, elevated SA levels substitute for light to maintain PhyB SUMOylation and immune-related photobody formation by stimulating the degradation of PhyB targeting deSUMOylase, OTS1. SUMOylated PhyB-NPR1 immune photobodies associate with TGA transcription factor associated chromatin to trigger immune gene expression. We unravel a mechanism where SUMOylation can enable light to recruit NPR1 to PhyB nuclear condensates to form immune photobodies to regulate plant immunity. HighlightsO_LILight-dependent immunity in plants relies on the SUMO mediated interaction between the photoreceptor PhyB and the Salicylic Acid (SA) receptor NPR1. C_LIO_LILight induced PhyB SUMOylation recruits NPR1 to nuclear condensates which we identify as immune photobodies that elevate SA levels for immune responses. C_LIO_LIIn darkness, SA can replace light in enabling PhyB-NPR1 immune photobody formation by regulating SUMOylation revealing a SA mediated mechanism for controlling PhyB liquid-liquid phase separation. C_LIO_LISUMO-modified PhyB-NPR1 immune photobodies regulate transcriptional activity of immune associated chromatin to shape defence responses in plants. C_LI