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SnRK1A 相互作用的负调控因子调节非生物胁迫下谷类幼苗源库通讯中养分饥饿信号传感器 SnRK1。

SnRK1A-interacting negative regulators modulate the nutrient starvation signaling sensor SnRK1 in source-sink communication in cereal seedlings under abiotic stress.

机构信息

Graduate Institute of Life Sciences, National Defense Medical Center, Neihu, Taipei 114, Taiwan, Republic of China.

出版信息

Plant Cell. 2014 Feb;26(2):808-27. doi: 10.1105/tpc.113.121939. Epub 2014 Feb 25.

Abstract

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.

摘要

在植物中,源库通讯在作物生产力中起着关键作用,但潜在的调节机制在很大程度上尚不清楚。SnRK1A 蛋白激酶和转录因子 MYBS1 调节谷类幼苗生长过程中的糖饥饿信号通路。在这里,我们鉴定了植物特异性的 SnRK1A 相互作用的负调控因子(SKINs)。SKINs 拮抗 SnRK1A 的功能,而高度保守的 GKSKSF 结构域对于 SKINs 作为抑制剂发挥作用是必不可少的。SKINs 的过表达抑制 MYBS1 的表达和胚乳中养分储备动员所必需的水解酶的表达,从而抑制幼苗生长。SKINs 的表达受干旱高度诱导,受各种胁迫中度诱导,这可能与胁迫下 ABA 介导的 SnRK1A 抑制有关。SKINs 的过表达增强了 ABA 对幼苗生长抑制的敏感性。ABA 促进了 SnRK1A 与 SKINs 之间的相互作用,并将 SKINs 的定位从细胞核转移到细胞质,在细胞质中,SKINs 结合 SnRK1A 并阻止 SnRK1A 和 MYBS1 进入细胞核。我们的研究结果表明,SnRK1A 在幼苗生长过程中调节源库通讯中起着关键作用。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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