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The FERONIA Receptor Kinase Maintains Cell-Wall Integrity during Salt Stress through Ca2+ Signaling

Current biology, 2018-03, Vol.28 (5), p.666-675.e5 [Peer Reviewed Journal]

2018 The Authors ;Attribution - NonCommercial - NoDerivatives ;ISSN: 0960-9822 ;EISSN: 1879-0445 ;DOI: 10.1016/j.cub.2018.01.023 ;PMID: 29456142

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  • Title:
    The FERONIA Receptor Kinase Maintains Cell-Wall Integrity during Salt Stress through Ca2+ Signaling
  • Author: Feng, Wei ; Kita, Daniel ; Peaucelle, Alexis ; Cartwright, Heather N. ; Doan, Vinh ; Duan, Qiaohong ; Liu, Ming-Che ; Maman, Jacob ; Steinhorst, Leonie ; Schmitz-Thom, Ina ; Yvon, Robert ; Kudla, Jörg ; Wu, Hen-Ming ; Cheung, Alice Y. ; Dinneny, José R.
  • Subjects: Ca2+ signaling ; cell-wall integrity ; cell-wall sensing ; FERONIA ; Life Sciences ; pectin ; root growth ; salt stress ; Vegetal Biology
  • Is Part Of: Current biology, 2018-03, Vol.28 (5), p.666-675.e5
  • Description: 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 di-glucose 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. [Display omitted] •FER is necessary to maintain cell-wall integrity during the salt-stress response•Pectin cross-linking protects cell walls against damage induced by salinity•The extracellular domain of FER interacts directly with pectin•FER induces cell-specific [Ca2+] transients that maintain cell-wall integrity For plant cells, growth requires maintenance of cell-wall integrity. Feng et al. show that salinity weakens the cell wall, which triggers FER-mediated calcium signaling to prevent root cells from bursting during growth under salt stress. The extracellular domain of FER physically interacts with pectin, indicating a potential sensing mechanism.
  • Publisher: Elsevier Inc
  • Language: English
  • Identifier: ISSN: 0960-9822
    EISSN: 1879-0445
    DOI: 10.1016/j.cub.2018.01.023
    PMID: 29456142
  • Source: Cell Press Free Archives
    Hyper Article en Ligne (HAL) (Open Access)
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