Résumé
Plant roots forage the soil for iron, the concentration of which can be dramatically lower than those needed for growth. Soil iron uptake uses the broad metal spectrum IRT1 transporter that also transports zinc, manganese, cobalt, and cadmium. Sophisticated iron-dependent transcriptional regulatory mechanisms allow plants to tightly control the abundance of IRT1, ensuring optimal absorption of iron. Here, we uncover that IRT1 acts as a transporter and receptor (transceptor), directly sensing excess of its non-iron metal substrates in the cytoplasm, to regulate its own degradation. Direct metal binding to a histidine-rich stretch in IRT1 triggers its phosphorylation by the CIPK23 kinase and facilitates the subsequent recruitment of the IDF1 E3 ligase. CIPK23-driven phosphorylation and IDF1-mediated lysine-63 polyubiquitination are jointly required for efficient endosomal sorting and vacuolar degradation of IRT1. Thus, IRT1 directly senses elevated non-iron metal concentrations and integrates multiple substrate-dependent regulations to optimize iron uptake and protect plants from highly reactive metals.
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•Soil metal excess is directly sensed by the IRT1 plant metal transporter-receptor•CIPK23 phosphorylates metal-loaded IRT1 and triggers its K63 polyUb by IDF1•K63 polyUb and phosphorylation are both required to target IRT1 to the vacuole•IRT1 vacuolar degradation limits the accumulation of highly reactive metals in plants
Plants protect themselves from highly reactive metals found in soils by tightly regulating the localization and the abundance of root metal transporters. Dubeaux et al. now report on the ability of the IRT1 transporter to directly sense metal excess and to initiate a response that culminates in IRT1 destruction.