SUMMARY Cells maintain integrity despite changes in their mechanical properties elicited during growth and environmental stress. How cells sense their physical state and compensate for cell-wall damage is poorly understood, particularly in plants. Here we report that FERONIA (FER), a plasma-membrane-localized receptor kinase from Arabidopsis, is necessary for the recovery of root growth after exposure to high salinity, a widespread soil stress. The extracellular domain of FER displays tandem regions of homology with malectin, an animal protein known to bind diglucose in vitro and important for protein quality control in the endoplasmic reticulum. The presence of malectin-like domains in FER and related receptor kinases has led to widespread speculation that they interact with cell-wall polysaccharides and can potentially serve a wall-sensing function. Results reported here show that salinity causes softening of the cell wall and that FER is necessary to sense these defects. When this function is disrupted in the fer mutant, root cells explode dramatically during growth recovery. Similar defects are observed in the mur1 mutant, which disrupts pectin cross-linking. Furthermore, fer cell-wall integrity defects can be rescued by treatment with calcium and borate, which also facilitate pectin cross-linking. Sensing of these salinity-induced wall defects might therefore be a direct consequence of physical interaction between the extracellular domain of FER and pectin. FER-dependent signaling elicits cell-specific calcium transients that maintain cell-wall integrity during salt stress. These results reveal a novel extracellular toxicity of salinity, and identify FER as a sensor of damage to the pectin-associated wall.

The significance of cell wall invertase (cwINV) for plant defense was investigated by comparing wild-type tobacco (Nicotiana tabacum) Samsun NN (SNN) with plants with RNA interference (RNAi)-mediated repression of cwINV (SNNTcwINV). In source leaves of SNNTcwINV, the activity of cwINV was repressed by about 90%. Sucrose export and apoplastic carbohydrate levels were significantly reduced, while photosynthesis and dark respiration exhibited little or no change. Activities of sucrose synthase and phosphofructokinase were depressed moderately, while ADP-glucose pyrophosphorylase was diminished greatly. Yet, the content of cytosolic/vacuolar carbohydrates was not significantly lower, which correlated with the absence of phenotypic effects in SNNTcwINV under normal growing conditions. By contrast, defense-related processes in primary metabolism and hypersensitive cell death were impaired and delayed in correlation with repression of cwINV. The increase in cwINV observed in source leaves of the resistant wild type following infection with Phytophthora nicotianae was absent in SNNTcwINV. Also, defense-related callose deposition at cell-to-cell interfaces, the related decline in sugar export, and accumulation of apoplastic carbohydrates were reduced and delayed. Expression of pathogenesis-related proteins and increase in phenylalanine ammonialyase and glucose-6-phosphate dehydrogenase activities were alleviated. Formation of hydrogen peroxide and development of hypersensitive lesions were weak and heterogeneous, and the pathogen was able to sporulate. We conclude that in photosynthetically active leaves of the apoplastic phloem loader, tobacco cwINV plays an essential role for acquisition of carbohydrates during plant-pathogen interactions and that the availability of these carbohydrates supports the onset of the hypersensitive reaction and ensures successful defense.

In plants, potassium (K ) homeostasis is tightly regulated and established against a concentration gradient to the environment. Despite the identification of Ca -regulated kinases as modulators of K channels, the immediate signaling and adaptation mechanisms of plants to low-K conditions are only partially understood. To assess the occurrence and role of Ca signals in Arabidopsis thaliana roots, we employed ratiometric analyses of Ca dynamics in plants expressing the Ca reporter YC3.6 in combination with patch-clamp analyses of root cells and two-electrode voltage clamp (TEVC) analyses in Xenopus laevis oocytes. K deficiency triggers two successive and distinct Ca signals in roots exhibiting spatial and temporal specificity. A transient primary Ca signature arose within 1 min in the postmeristematic stelar tissue of the elongation zone, while a secondary Ca response occurred after several hours as sustained Ca elevation in defined tissues of the elongation and root hair differentiation zones. Patch-clamp and TEVC analyses revealed Ca dependence of the activation of the K channel AKT1 by the CBL1-CIPK23 Ca sensor-kinase complex. Together, these findings identify a critical role of cell group-specific Ca signaling in low K responses and indicate an essential and direct role of Ca signals for AKT1 K channel activation in roots.

both species were analyzed during exposure to hyperpolarization/depolarization cycles or in response to application of the amino acid glutamate. We found a superior performance of the UBQ10 promoter with regard to expression pattern, levels and expression stabilities in both species. We observed remarkable differences between the two species in the spatiotemporal parameters of the observed Ca 2+ signatures.Rice appeared in general to respond with a lower maximal signal amplitude but greatly increased signal duration when compared with Arabidopsis. Our results identify important advantages to using the UBQ10 promoter in Arabidopsis and rice and in T-DNA mutant backgrounds. Moreover, the observed differences in Ca 2+ signaling in the two species underscore the need for comparative studies to achieve a comprehensive understanding of Ca 2+ signaling in plants.

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