TY - JOUR AB - Availability of the essential macronutrient nitrogen in soil plays a critical role in plant growth, development, and impacts agricultural productivity. Plants have evolved different strategies for sensing and responding to heterogeneous nitrogen distribution. Modulation of root system architecture, including primary root growth and branching, is among the most essential plant adaptions to ensure adequate nitrogen acquisition. However, the immediate molecular pathways coordinating the adjustment of root growth in response to distinct nitrogen sources, such as nitrate or ammonium, are poorly understood. Here, we show that growth as manifested by cell division and elongation is synchronized by coordinated auxin flux between two adjacent outer tissue layers of the root. This coordination is achieved by nitrate‐dependent dephosphorylation of the PIN2 auxin efflux carrier at a previously uncharacterized phosphorylation site, leading to subsequent PIN2 lateralization and thereby regulating auxin flow between adjacent tissues. A dynamic computer model based on our experimental data successfully recapitulates experimental observations. Our study provides mechanistic insights broadening our understanding of root growth mechanisms in dynamic environments. AU - Ötvös, Krisztina AU - Marconi, Marco AU - Vega, Andrea AU - O’Brien, Jose AU - Johnson, Alexander J AU - Abualia, Rashed AU - Antonielli, Livio AU - Montesinos López, Juan C AU - Zhang, Yuzhou AU - Tan, Shutang AU - Cuesta, Candela AU - Artner, Christina AU - Bouguyon, Eleonore AU - Gojon, Alain AU - Friml, Jiří AU - Gutiérrez, Rodrigo A. AU - Wabnik, Krzysztof T AU - Benková, Eva ID - 9010 IS - 3 JF - EMBO Journal SN - 02614189 TI - Modulation of plant root growth by nitrogen source-defined regulation of polar auxin transport VL - 40 ER - TY - JOUR AB - CLC chloride/proton exchangers may support acidification of endolysosomes and raise their luminal Cl− concentration. Disruption of endosomal ClC‐3 causes severe neurodegeneration. To assess the importance of ClC‐3 Cl−/H+ exchange, we now generate Clcn3unc/unc mice in which ClC‐3 is converted into a Cl− channel. Unlike Clcn3−/− mice, Clcn3unc/unc mice appear normal owing to compensation by ClC‐4 with which ClC‐3 forms heteromers. ClC‐4 protein levels are strongly reduced in Clcn3−/−, but not in Clcn3unc/unc mice because ClC‐3unc binds and stabilizes ClC‐4 like wild‐type ClC‐3. Although mice lacking ClC‐4 appear healthy, its absence in Clcn3unc/unc/Clcn4−/− mice entails even stronger neurodegeneration than observed in Clcn3−/− mice. A fraction of ClC‐3 is found on synaptic vesicles, but miniature postsynaptic currents and synaptic vesicle acidification are not affected in Clcn3unc/unc or Clcn3−/− mice before neurodegeneration sets in. Both, Cl−/H+‐exchange activity and the stabilizing effect on ClC‐4, are central to the biological function of ClC‐3. AU - Weinert, Stefanie AU - Gimber, Niclas AU - Deuschel, Dorothea AU - Stuhlmann, Till AU - Puchkov, Dmytro AU - Farsi, Zohreh AU - Ludwig, Carmen F. AU - Novarino, Gaia AU - López-Cayuqueo, Karen I. AU - Planells-Cases, Rosa AU - Jentsch, Thomas J. ID - 7586 JF - EMBO Journal SN - 02614189 TI - Uncoupling endosomal CLC chloride/proton exchange causes severe neurodegeneration VL - 39 ER -