Higher plants take up nutrients via the roots and load them into xylem vessels for translocation to the shoot. After uptake, anions have to be channeled toward the root xylem vessels. Thereby, xylem parenchyma and pericycle cells control the anion composition of the root-shoot xylem sap [1-6]. The fact that salt-tolerant genotypes possess lower xylem-sap Cl(-) contents compared to salt-sensitive genotypes [7-10] indicates that membrane transport proteins at the sites of xylem loading contribute to plant salinity tolerance via selective chloride exclusion. However, the molecular mechanism of xylem loading that lies behind the balance between NO3(-) and Cl(-) loading remains largely unknown. Here we identify two root anion channels in Arabidopsis, SLAH1 and SLAH3, that control the shoot NO3(-)/Cl(-) ratio. The AtSLAH1 gene is expressed in the root xylem-pole pericycle, where it co-localizes with AtSLAH3. Under high soil salinity, AtSLAH1 expression markedly declined and the chloride content of the xylem sap in AtSLAH1 loss-of-function mutants was half of the wild-type level only. SLAH3 anion channels are not active per se but require extracellular nitrate and phosphorylation by calcium-dependent kinases (CPKs) [11-13]. When co-expressed in Xenopus oocytes, however, the electrically silent SLAH1 subunit gates SLAH3 open even in the absence of nitrate- and calcium-dependent kinases. Apparently, SLAH1/SLAH3 heteromerization facilitates SLAH3-mediated chloride efflux from pericycle cells into the root xylem vessels. Our results indicate that under salt stress, plants adjust the distribution of NO3(-) and Cl(-) between root and shoot via differential expression and assembly of SLAH1/SLAH3 anion channel subunits.
As the major sugar-producing crop in Europe and North America, sugar beet (Beta vulgaris) taproots store sucrose at a concentration of about 20 %. While the TST sucrose transporter, which drives vacuolar sugar accumulation in the taproot, has already been identified, sugar transporters mediating sucrose uptake across the plasma membrane of taproot parenchyma cells remained unknown. We electrophysiologically examined taproots for proton-coupled sugar uptake and identified potentially involved transporters by transcriptomic profiling. After cloning, the transporter features were studied in the heterologous Xenopus laevis oocyte expression system using the two-electrode voltage clamp technique. Insights into the structure was gained by 3D homology modeling. As with glucose, sucrose stimulation of taproot parenchyma cells caused inward proton fluxes and plasma membrane depolarization, indicating a sugar/proton symport mechanism. As one potential candidate for sugar uploading, the BvPMT5a was characterized as a H+-driven low-affinity glucose transporter, which does not transport sucrose. BvSTP13 operated as a high-affinity H+/sugar symporter, transporting glucose and to some extent sucrose due to a binding cleft plasticity, and was more cold-resistant than BvPMT5a. Identification of BvPMT5a and BvSTP13 as taproot sugar transporters could improve breeding of cold-tolerant sugar beet to provide a sustainable energy crop.
GABA, a molecule involved in the regulation of the stomata aperture and drought tolerance does not modify vacuolar anion fluxes mediated by the anion channel AtALMT9.
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