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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

机译:snRK1a-Interacting Negative Regulators modulate the Nutrient starvation signaling sensor snRK1 in source-sink Communication in Cereal seedlings under abiotic stress

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摘要

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.
机译:在植物中,源库沟通在作物生产力中起着举足轻重的作用,但基本的调控机制尚不清楚。 SnRK1A蛋白激酶和转录因子MYBS1调节谷物幼苗生长过程中的糖饥饿信号传导途径。在这里,我们确定了植物特异的SnRK1A相互作用负调节剂(SKINs)。 SKIN拮抗SnRK1A的功能,高度保守的GKSKSF结构域对于SKIN发挥阻遏作用至关重要。 SKINs的过表达抑制了胚乳中动员养分储备所必需的MYBS1和水解酶的表达,从而抑制了幼苗的生长。 SKINs的表达在干旱和各种胁迫下均是高度诱导的,这可能与脱落酸(ABA)介导的胁迫下SnRK1A的抑制有关。 SKINs的过表达增强了ABA敏感性,可抑制幼苗生长。 ABA促进SnRK1A与SKIN之间的相互作用,并将SKIN的定位从细胞核转移到细胞质,并与SnRK1A结合并阻止SnRK1A和MYBS1进入细胞核。我们的发现表明,SnRK1A在幼苗生长过程中起着调节源库沟通的关键作用。在非生物胁迫下,SKINs拮抗SnRK1A的功能,这可能是限制幼苗活力的关键因素。

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