Another brick in the mall igg1/9/2024 Within the indentation range used (less than 500 nm Figure S4B), the force-by-indentation curves of both turgid and plasmolyzed cells similarly fit a paraboloid model ( Figures S4C and S4D), suggesting that there was minimal contribution from cellular turgor within our measurements. Here, the surface wall of epidermal cells was of greatest interest, because we observed rupturing of cells in this region therefore, un-plasmolyzed roots were used (see STAR Methods). Taken together, these data reveal that FER promotes growth recovery and seedling survival during salt stress, most likely by maintaining cell-wall integrity. We also traced the volume change of fer epidermal cells and found a rapid increase before cell bursting ( Figure S2C), suggesting that excessive loosening of the wall may cause the loss of cell integrity. In contrast, whereas a few epidermal cells in WT also lost cell integrity after salt treatment, the frequency was much lower and was rarely observed in cortical cells ( Figure 2G). Tissue-specific quantification of these events in fer seedlings revealed that cells in the epidermal and cortical layers showed a loss of cell integrity starting 3–4 hr after the beginning of salt treatment and peaking in frequency by 7–8 hr ( Figure 2H Figures S2A and S2B). Cell bursting occurred to such an extent that it sometimes caused a complete loss of intact cells in the outer tissues of the growth zone ( Figure 2F). In the fer mutant, a similar loss of expansion anisotropy was initiated but quickly followed by rupturing of cells (seen as a break in the continuity of the plasma-membrane marker, and subsequently a loss of YFP fluorescence Figures 2D–2F Movie S1). ![]() These results reveal a novel extracellular toxicity of salinity, and identify FER as a sensor of damage to the pectin-associated wall. FER-dependent signaling elicits cell-specific calcium transients that maintain cell-wall integrity during salt stress. Sensing of these salinity-induced wall defects might therefore be a direct consequence of physical interaction between the extracellular domain of FER and pectin. Furthermore, fer cell-wall integrity defects can be rescued by treatment with calcium and borate, which also facilitate pectin cross-linking. Similar defects are observed in the mur1 mutant, which disrupts pectin cross-linking. When this function is disrupted in the fer mutant, root cells explode dramatically during growth recovery. Results reported here show that salinity causes softening of the cell wall and that FER is necessary to sense these defects. 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. The extracellular domain of FER displays tandem regions of homology with malectin, an animal protein known to bind di-glucose in vitro and important for protein quality control in the endoplasmic reticulum. ![]() 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. How cells sense their physical state and compensate for cell-wall damage is poorly understood, particularly in plants. ![]() Cells maintain integrity despite changes in their mechanical properties elicited during growth and environmental stress.
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