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SnRK1A-Interacting Negative Regulators Modulate the Nutrient Starvation Signaling Sensor SnRK1 in Source-Sink Communication in Cereal Seedlings under Abiotic Stress

By C.-R. Lin, K.-W. Lee, C.-Y. Chen, Y.-F. Hong, J.-L. Chen, C.-A. Lu, K.-T. Chen, T.-H. D. Ho and S.-M. Yu


In plants, source-sink communication plays a pivotal role in crop productivity, yet the underlying regulatory mechanisms are largely unknown. The SnRK1A protein kinase and transcription factor MYBS1 regulate the sugar starvation signaling pathway during seedling growth in cereals. Here, we identified plant-specific SnRK1A-interacting negative regulators (SKINs). SKINs antagonize the function of SnRK1A, and the highly conserved GKSKSF domain is essential for SKINs to function as repressors. Overexpression of SKINs inhibits the expression of MYBS1 and hydrolases essential for mobilization of nutrient reserves in the endosperm, leading to inhibition of seedling growth. The expression of SKINs is highly inducible by drought and moderately by various stresses, which is likely related to the abscisic acid (ABA)-mediated repression of SnRK1A under stress. Overexpression of SKINs enhances ABA sensitivity for inhibition of seedling growth. ABA promotes the interaction between SnRK1A and SKINs and shifts the localization of SKINs from the nucleus to the cytoplasm, where it binds SnRK1A and prevents SnRK1A and MYBS1 from entering the nucleus. Our findings demonstrate that SnRK1A plays a key role regulating source-sink communication during seedling growth. Under abiotic stress, SKINs antagonize the function of SnRK1A, which is likely a key factor restricting seedling vigor

Topics: Abscisic Acid, Amino Acid Sequence, Carbohydrate Metabolism, Cell Hypoxia, Cell Nucleus, Conserved Sequence, Endosperm, Gene Expression Regulation, Plant, Hordeum, Models, Biological, Molecular Sequence Data, Multigene Family, Oryza sativa, Plant Proteins, Protein Binding, Protein Structure, Tertiary, Protein Transport, Protein-Serine-Threonine Kinases, Seedling, Starch, Signal Transduction, Stress, Physiological
Year: 2015
DOI identifier: 10.1105/tpc.113.121939
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