Modulators of the Abscisic Acid Core Signaling Pathway

脱落酸核心信号通路的调节剂

• 批准号: 1558011
• 负责人: Ruth Finkelstein
• 金额: $ 49.97万
• 依托单位: University of California-Santa Barbara
• 依托单位国家: 美国
• 项目类别: Continuing Grant
• 财政年份: 2016
• 资助国家: 美国
• 起止时间: 2016-07-15 至 2023-09-30
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=1558011&HistoricalAwards=false
• 关键词: Modulators; Abscisic; Acid; Core; Signaling

Increases in the human population of the Earth, coupled with increased carbon emissions, are leading to changes in our global climate that threaten agriculture just as our collective demands grow. Climate change is manifest as severe weather events ranging from warming and drought to major storms and flooding in different regions. The combination of severe drought during growing seasons and excessive moisture during cereal grain maturation can lead to many billions of dollars in annual yield losses worldwide. A better understanding of the genetic mechanisms controlling plant stress tolerance and productivity could help us to create or breed plants that could better withstand unfavorable climate events. The hormone abscisic acid (ABA) is a key regulator of stress signaling. Within the last seven years a "core ABA signaling pathway" has emerged that mechanistically links many ABA signaling components that were previously identified genetically. This proposal addresses the function of a group of proteins that interact directly with multiple central components of this core pathway, possibly functioning as signaling hubs. Understanding the interactions controlling ABA responses could be instrumental for ensuring the world's future food security. The central components of the ABA core signaling pathway include four families of proteins: the PYL/PYR/RCAR family of ABA receptors, the clade A family of protein phosphatase (PP)2Cs, the Snf-Related Kinase (SnRK)2 family,and the ABI5/ABF/AREB clade of ABA response element binding basic leucine zipper (bZIP) class transcription factors. An additional family, the ABI Five binding Protein (AFP)s, interact directly with the bZIPs, PP2Cs and SnRK2s, and also show interactions with chromatin modifiers. This project will address the mechanisms and implications of these interactions by determining 1) whether AFPs act as transcriptional repressors of ABA response element (ABRE)-containing genes by sequestering bZIPs at low ABA concentrations; (2) whether AFPs interact with TPL-like co-repressor(s) or other chromatin modifying protein(s) to alter histone acetylation and activity of genes regulated by bZIPs; and 3) whether AFP function and localization is regulated by changes in phosphorylation mediated by PP2Cs and SnRK2s or other kinases. The proposed experiments will test how the AFPs contribute to a feedback system that permits plants to resume growth when developmentally or stress-induced ABA levels decline. In addition, they will address the biochemical function(s) of a family still annotated only as proteins of unknown function.

地球人口的增加，加上碳排放的增加，正在导致我们的全球气候变化，在我们的集体需求增长之际，这些变化威胁着农业。气候变化表现为不同地区的恶劣天气事件，从变暖和干旱到大风暴和洪水。生长季节的严重干旱和谷物成熟期间的过多水分相结合，可能导致全球每年数十亿美元的产量损失。更好地了解控制植物耐逆性和生产力的遗传机制，可以帮助我们创造或培育能够更好地抵御不利气候事件的植物。激素脱落酸(ABA)是胁迫信号的关键调节因子。在过去的七年里，一个“核心ABA信号通路”已经出现，它机械地连接了许多以前从遗传上确定的ABA信号成分。这一建议解决了一组蛋白质的功能，这些蛋白质直接与这一核心途径的多个中心组件相互作用，可能起到信号枢纽的作用。了解控制ABA反应的相互作用可能有助于确保世界未来的粮食安全。ABA核心信号通路的核心成分包括四个蛋白质家族：ABA受体PYL/PYR/RCAR家族、蛋白磷酸酶(PP)2Cs家族、SNF相关激酶(SnRK)2家族和ABA反应元件结合碱性亮氨酸拉链(BZIP)类转录因子的ABI5/ABF/AREB家族。另外一个家族，ABI5结合蛋白S，直接与bZIP、PP2Cs和SnRK2相互作用，也与染色质修饰物相互作用。这个项目将通过确定1)AFP是否通过在低ABA浓度下隔离bZIP而作为含ABA反应元件(ABRE)基因的转录抑制物；(2)AFP是否与TPL样共抑制子(S)或其他染色质修饰蛋白(S)相互作用来改变组蛋白乙酰化和受bZIP调控的基因的活性；以及3)AFP的功能和定位是否受PP2Cs和SnRK2或其他激酶介导的磷酸化变化的调节。拟议的实验将测试AFP如何有助于反馈系统，该系统允许植物在发育或压力诱导的ABA水平下降时恢复生长。此外，他们将讨论一个家族的生化功能(S)，这个家族仍然只被注释为功能未知的蛋白质。

项目成果

ABI5-binding proteins (AFPs) alter transcription of ABA-induced genes via a variety of interactions with chromatin modifiers

• DOI: 10.1007/s11103-016-0569-1
• 发表时间: 2017-03-01
• 期刊: PLANT MOLECULAR BIOLOGY
• 影响因子: 5.1
• 作者: Lynch, Tim J.;Erickson, B. Joy;Finkelstein, Ruth R.
• 通讯作者: Finkelstein, Ruth R.