Nls mcherry snapgene1/6/2024 The latter response is intertwined with the defense pathways since the inflammatory Interleukine-6 pathway directly interacts with the BMPR complex to regulate iron uptake genes 4. Systemically, TfR activation triggers stimulation of the BMPR complex to increase the expression of iron uptake genes 4. Locally, the loss of iron induces TfR endocytosis and intracellular iron storage via ferritins. Upon host–pathogen interaction, bacterial siderophores outcompete the host iron-bound to transferrin, which in turn leads to a loss of iron triggering independent local and systemic responses in the host 4. In mammals, two receptors, transferrin receptor 1 and 2 (TfR), which bind extracellular transferrin-associated iron, play a major role in regulating external iron sensing and homeostasis 3. Thus, host external iron sensing and internal iron homeostasis regulation are of particular importance to prevent pathogen infection, and are part of the first line of defense called nutritional immunity 3. Pathogens scavenge iron from the host through siderophore secretion while the host aims to sequester iron to prevent pathogen virulence. In plants, Graminaceae species employ plant specific siderophores while non-Graminaceae such as Arabidopsis thaliana depend on an iron reduction-based uptake strategy 2.ĭuring pathogen attack, iron is at the nexus of host–pathogen interaction as both organisms compete for this metal. Mammals acquire iron mainly through the glycoprotein transferrin while bacteria, fungi and plants have evolved diverse systems that include siderophores, which are small, high-affinity diffusible secondary metabolites that chelate Fe 3+ from the surrounding environment 1. Organisms have evolved efficient iron uptake mechanisms that include a variety of membrane-associated systems that absorb iron unbound or bound to iron-binding molecules 1. While iron is very abundant in the Earth’s crust, its bioavailability is low. Iron is a critical micronutrient for all living organisms. We propose that SRF3 is part of nutritional immunity responses involved in sensing external iron levels. Mimicking bacterial elicitation with the flagellin peptide flg22 phenocopies SRF3 regulation upon low iron levels and subsequent SRF3-dependent responses. 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. Here we report a receptor kinase SRF3, with a role in coordinating root growth, iron homeostasis and immunity pathways via regulation of callose synthases. 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. Thus, iron sensing and homeostasis are of particular importance to prevent host infection and part of nutritional immunity. While pathogens seek to scavenge iron to spread, the host aims at decreasing iron availability to reduce pathogen virulence. Iron is critical for host–pathogen interactions. Nature Communications volume 13, Article number: 4445 ( 2022) The receptor kinase SRF3 coordinates iron-level and flagellin dependent defense and growth responses in plants
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