Journal
NATURE
Volume 572, Issue 7769, Pages 341-+Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41586-019-1449-z
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Funding
- Shenzhen Peacock Innovative Research Team Program
- Pandeng Project of Hangzhou Normal University
- Chinese NSF [31301170, U1130304]
- China Scholarship Council
- NSF [IOS-1457257, IOS-0848263]
- USDA [CSREES-2006-35100-17304]
- National Key Project for Synthetic Biology [2018YFA0902500]
- DOE [DE-SC0014077]
- U.S. Department of Energy (DOE) [DE-SC0014077] Funding Source: U.S. Department of Energy (DOE)
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Salinity is detrimental to plant growth, crop production and food security worldwide. Excess salt triggers increases in cytosolic Ca2+ concentration, which activate Ca2+-binding proteins and upregulate the Na+/H+ antiporter in order to remove Na+. Salt-induced increases in Ca2+ have long been thought to be involved in the detection of salt stress, but the molecular components of the sensing machinery remain unknown. Here, using Ca2+-imaging-based forward genetic screens, we isolated the Arabidopsis thaliana mutant monocation-induced [Ca2+](i) increases 1 (moca1), and identified MOCA1 as a glucuronosyltransferase for glycosyl inositol phosphorylceramide (GIPC) sphingolipids in the plasma membrane. MOCA1 is required for salt-induced depolarization of the cell-surface potential, Ca2+ spikes and waves, Na+/H+ antiporter activation, and regulation of growth. Na+ binds to GIPCs to gate Ca2+ influx channels. This salt-sensing mechanism might imply that plasma-membrane lipids are involved in adaption to various environmental salt levels, and could be used to improve salt resistance in crops.
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