Calcium can ameliorate Na+ toxicity in plants by decreasing Na+ influx through nonselective cation channels. Here, we show that elevated external [Ca2+] also inhibits Na+-induced K+ efflux through outwardly directed, K+-permeable channels. Noninvasive ion flux measuring and patch-clamp techniques were used to characterize K+ fluxes from Arabidopsis (Arabidopsis thaliana) root mature epidermis and leaf mesophyll under various Ca2+ to Na+ ratios. NaCl-induced K+ efflux was not related to the osmotic component of the salt stress, was inhibited by the K+ channel blocker TEA+, was not mediated by inwardly directed K+ channels (tested in the akt1 mutant), and resulted in a significant decrease in cytosolic K+ content. NaCl-induced K+ efflux was partially inhibited by 1 mm Ca2+ and fully prevented by 10 mm Ca2+. This ameliorative effect was at least partially attributed to a less dramatic NaCl-induced membrane depolarization under high Ca2+ conditions. Patch-clamp experiments (whole-cell mode) have demonstrated that two populations of Ca2+-sensitive K+ efflux channels exist in protoplasts isolated from the mature epidermis of Arabidopsis root and leaf mesophyll cells. The instantaneously activating K+ efflux channels showed weak voltage dependence and insensitivity to external and internal Na+. Another population of K+ efflux channels was slowly activating, steeply rectifying, and highly sensitive to Na+. K+ efflux channels in roots and leaves showed different Ca2+ and Na+ sensitivities, suggesting that these organs may employ different strategies to withstand salinity. Our results suggest an additional mechanism of Ca2+ action on salt toxicity in plants: the amelioration of K+ loss from the cell by regulating (both directly and indirectly) K+ efflux channels.

Growth regulation tailors plant development to its environment. A showcase is response to gravity, where shoots bend up and roots down 1 . This paradox is based on opposite effects of the phytohormone auxin, which promotes cell expansion in shoots, while inhibiting it in roots via a yet unknown cellular mechanism 2 . Here, by combining micro uidics, live imaging, genetic engineering and phosphoproteomics in Arabidopsis thaliana, we advance our understanding how auxin inhibits root growth. We show that auxin activates two distinct, antagonistically acting signalling pathways that converge on the rapid regulation of the apoplastic pH, a causative growth determinant. Cell surface-based TRANSMEMBRANE KINASE1 (TMK1) interacts with and mediates phosphorylation and activation of plasma membrane H + -ATPases for apoplast acidi cation, while intracellular canonical auxin signalling promotes net cellular H + -in ux, causing apoplast alkalinisation. The simultaneous activation of these two counteracting mechanisms poises the root for a rapid, ne-tuned growth modulation while navigating complex soil environment. MainAuxin, a major growth regulator in plants, acts oppositely in shoots and roots. In shoots, canonical/intracellular auxin TRANSPORT INHIBITOR RESPONSE1 (TIR1)/AUXIN-SIGNALING F-BOX (AFB) receptors by downstream transcriptional regulation activate H + -pumps to acidify the apoplast a promote cell elongation 3,4 , in accordance with the Acid Growth Theory, which postulates that low apoplastic pH promotes growth 5 . In roots of many species including Arabidopsis, auxin inhibits growth. These contrasting responses are the basis for positive versus negative bending of roots and shoots in response to gravity and light 1 . The inhibitory auxin effect in roots also involves TIR1/AFB receptors but its rapid timing points towards an unknown non-transcriptional signalling branch 6 . Besides, a cell surface-based pathway involving TMK1 regulates development 7 , including differential growth in the apical hook 8 , while its role in auxin-regulated root growth remains unclear. Hence, the auxin signalling mechanism and the downstream processes for regulating root growth remain elusive.In this study, we revealed antagonistic action of intracellular TIR1/AFB and cell surface TMK1 auxin signalling converging on regulation of apoplastic pH, which we con rm as the key cellular mechanism allowing immediate and sensitive root growth regulation. Growth inhibition correlates with H + -in uxAuxin rapidly inhibits root growth through a non-transcriptional branch of TIR1/AFB signalling 6 . Although several cellular processes, including cortical microtubule (CMT) reorientation 9,10 , vacuolar fragmentation 11 and apoplastic pH changes [12][13][14] have been implicated, the causal mechanism remains unidenti ed.

Chenopodium quinoa is a halophytic pseudocereal crop that is being cultivated in an ever-growing number of countries. Because quinoa is highly resistant to multiple abiotic stresses and its seed has a better nutritional value than any other major cereals, it is regarded as a future crop to ensure global food security. We generated a high-quality genome draft using an inbred line of the quinoa cultivar Real. The quinoa genome experienced one recent genome duplication about 4.3 million years ago, likely reflecting the genome fusion of two Chenopodium parents, in addition to the γ paleohexaploidization reported for most eudicots. The genome is highly repetitive (64.5% repeat content) and contains 54 438 protein-coding genes and 192 microRNA genes, with more than 99.3% having orthologous genes from glycophylic species. Stress tolerance in quinoa is associated with the expansion of genes involved in ion and nutrient transport, ABA homeostasis and signaling, and enhanced basal-level ABA responses. Epidermal salt bladder cells exhibit similar characteristics as trichomes, with a significantly higher expression of genes related to energy import and ABA biosynthesis compared with the leaf lamina. The quinoa genome sequence provides insights into its exceptional nutritional value and the evolution of halophytes, enabling the identification of genes involved in salinity tolerance, and providing the basis for molecular breeding in quinoa.