The receptor kinase SRF3 coordinates iron-level and flagellin dependent defense and growth responses in plants

Abstract

Iron is critical for host–pathogen interactions. While pathogens seek to scavenge iron to spread, the host aims at decreasing iron availability to reduce pathogen virulence. Thus, iron sensing and homeostasis are of particular importance to prevent host infection and part of nutritional immunity. While the link between iron homeostasis and immunity pathways is well established in plants, how iron levels are sensed and integrated with immune response pathways remains unknown. Here we report a receptor kinase SRF3, with a role in coordinating root growth, iron homeostasis and immunity pathways via regulation of callose synthases. These processes are modulated by iron levels and rely on SRF3 extracellular and kinase domains which tune its accumulation and partitioning at the cell surface. Mimicking bacterial elicitation with the flagellin peptide flg22 phenocopies SRF3 regulation upon low iron levels and subsequent SRF3-dependent responses. We propose that SRF3 is part of nutritional immunity responses involved in sensing external iron levels.

Ubiquitination steers SRF3 plasma membrane nano-organization to specify signaling outputs

“…Recently, we had found that SRF3 is critical in regulating the root growth response to low iron levels and to the bacterial peptide flagellin 22 (flg22) 27 . Under both conditions SRF3 is rapidly degraded from the plasma membrane (Supplementary Data 1a) 27 . We set out to explore by which cellular mechanism SRF3 is degraded from this compartment.…”

“…Since we had previously demonstrated that SRF3 is at the nexus of signaling pathways that are triggered in response to low iron levels and bacterial elicitation by flg 22 27 , we wondered whether SRF3 degradation is required to mediate signaling upon both signals. We first dissected whether SRF3 regulates low iron and flg22 root growth through a common or through independent signaling pathways.…”

“…Taken together, SRF3 accumulates along the endocytic pathway under unstressed conditions. As low iron conditions and treatment with flg22 cause a rapid removal of SRF3 from the plasma membrane 27 , we wanted to test whether this decrease could be caused by an increase of SRF3 endocytosis-triggered vacuolar targeting. We therefore evaluated the size of the BFA body as a proxy to evaluate the enrichment of SRF3 in EE/TGN 10 .…”

“…Iron homeostasis and defense pathways are tightly intertwined in eukaryotes given the micronutrient iron is critical for determining host-pathogen interactions 24 . Iron has been proposed to be involved in mediating host nutritional immunity and as a priming signal to initiate host defense responses [25][26][27][28][29] . The STRUBBELIG-RECEPTOR FAMILY 3 (SRF3) LRR-RK has been recently shown to mediate low iron and flg22-dependent root growth and transcriptional signaling, placing this receptor at the nexus of both pathways 27 .…”

“…The STRUBBELIG-RECEPTOR FAMILY 3 (SRF3) LRR-RK has been recently shown to mediate low iron and flg22-dependent root growth and transcriptional signaling, placing this receptor at the nexus of both pathways 27 . An important part of the SRF3 signaling mechanism is its decreased abundance at the plasma membrane in response to low iron and flg22-derived signals 27 . Here, we present the molecular mechanism by which SRF3 can trigger specific signaling pathways and how it relates to it abundance and localization at the plasma membrane.…”