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A Receptor-Like Kinase Mediates Ammonium Homeostasis and Is Important for the Polar Growth of Root Hairs in Arabidopsis

Ammonium (NH₄⁺) is both a necessary nutrient and an important signal in plants, but can be toxic in excess. Ammonium sensing and regulatory mechanisms in plant cells have not been fully elucidated. To decipher the complex network of NH₄⁺ signaling, we analyzed [Ca²⁺]cyt-associated protein kinase (CA...

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Published in:The Plant cell 2014-04, Vol.26 (4), p.1497-1511
Main Authors: Bai, Ling, Ma, Xiaonan, Zhang, Guozeng, Song, Shufei, Zhou, Yun, Gao, Lijie, Miao, Yuchen, Song, Chun-Peng
Format: Article
Language:English
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Summary:Ammonium (NH₄⁺) is both a necessary nutrient and an important signal in plants, but can be toxic in excess. Ammonium sensing and regulatory mechanisms in plant cells have not been fully elucidated. To decipher the complex network of NH₄⁺ signaling, we analyzed [Ca²⁺]cyt-associated protein kinase (CAP) genes, which encode signaling components that undergo marked changes in transcription levels in response to various Stressors. We demonstrated that CAP1, a tonoplast-localized receptor-like kinase, regulates root hair tip growth by maintaining cytoplasmic Ca²⁺ gradients. A CAP1 knockout mutant (cap1-1) produced elevated levels of cytoplasmic NH₄⁺. Furthermore, root hair growth of cap1-1 was inhibited on Murashige and Skoog medium, but NH₄⁺ depletion reestablished the Ca²⁺ gradient necessary for normal growth. The lower net NH₄⁺ influx across the vacuolar membrane and relatively alkaline cytosolic pH of cap1-1 root hairs implied that mutation of CAP1 increased NH₄⁺ accumulation in the cytoplasm. Furthermore, CAP1 functionally complemented the npr1 (nitrogen permease reactivator protein) kinase yeast mutant, which is defective in high-affinity NH₄⁺ uptake via MEP2 (methylammonium permease 2), distinguishing CAP1 as a cytosolic modulator of NH₄⁺ levels that participates in NH₄⁺ homeostasis-regulated root hair growth by modulating tip-focused cytoplasmic Ca²⁺ gradients.
ISSN:1040-4651
1532-298X
DOI:10.1105/tpc.114.124586