SOS1 safeguards plant circadian rhythm against daily salt fluctuations.
SOS1 safeguards plant circadian rhythm against daily salt fluctuations.
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DOI:
10.1073/pnas.2212950119
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发表时间:
2022-09-06
影响因子:
11.1
通讯作者:
中科院分区:
文献类型:
--
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The rotation of the Earth has generated cyclic changes in environmental factors. To fully exploit these predictable oscillatory factors for better fitness, plants have evolved an intricate endogenous timing system called the circadian clock. The plant circadian clock system perceives environmental cues like light and temperature through its input pathways. The input pathways then deliver these environmental cues to the core oscillators which are composed of interlocked transcription–translation feedback loops, generating self-sustaining circadian rhythms in various physiological processes through the output pathways (1, 2). Since most of the core oscillators are transcription factors, the plant circadian clock influences global transcription profoundly. Comprehensive transcriptomic studies suggest that 89% of transcripts in Arabidopsis cycle under certain conditions and the circadian clock system is responsible for the oscillatory expression of more than one-third of the genes in Arabidopsis (3). Strikingly, a study on plant transcriptome changes in response to salt, osmotic, and cold stresses suggests that 68% of the circadian oscillatory genes are involved in stress responses (4). It is now increasingly clear that the plant circadian clock plays an indispensable role in diverse plant stress responses (5). In PNAS, Cha et al. discover that SALT OVERLY SENSITIVE 1 (SOS1), a plasma membrane (PM) Na+/H+ antiporter, interacts with and stabilizes GIGANTEA (GI), a core circadian clock component, to realize period compensation of plant circadian clock under daily fluctuating salt levels (6). Due to inappropriate irrigation practices, misuse of fertilizer, and industrial pollution, salt stress has become one of the major hurdles curbing the yield of various crops, affecting over 6% of the world’s total land area (7). In response to the ionic toxicity triggered by salt stress, plants rely on the SOS pathway to transport excessive Na+ from the cytoplasm to the apoplast, thus ensuring endogenous ionic homeostasis. Although the bona fide sensor of Na+ is yet to be identified in plants, elevated intracellular and intercellular Na+ levels were found to trigger cytosolic Ca2+ signals, which are decoded by SOS3, an EF-hand Ca2+-binding protein. SOS3 interacts with and activates SOS2, a serine/threonine protein kinase, in a Ca2+-dependent manner. Activated SOS2 then phosphorylates SOS1, which releases the inhibition by the C-terminal autoinhibitory domain of SOS1, activating the Na+/H+ antiporter activity of SOS1. SOS1 transports excessive Na+ outward of the cytoplasm in exchange for inward transportation of H+. The H+ gradient across the PM which drives the activity of SOS1 is generated by PM H+-ATPase activated by salt stress (8).
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