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热休克因子 A8a 调节类黄酮合成和耐旱性。

HEAT SHOCK FACTOR A8a Modulates Flavonoid Synthesis and Drought Tolerance.

机构信息

State Key Laboratory of Crop Biology, College of Horticulture Sciences, Shandong Agricultural University, 271018 Tai'an, Shandong, China.

State Key Laboratory of Crop Biology, College of Horticulture Sciences, Shandong Agricultural University, 271018 Tai'an, Shandong, China

出版信息

Plant Physiol. 2020 Nov;184(3):1273-1290. doi: 10.1104/pp.20.01106. Epub 2020 Sep 21.

Abstract

Drought is an important environmental factor affecting the growth and production of agricultural crops and fruits worldwide, including apple (). Heat shock factors (HSFs) have well-documented functions in stress responses, but their roles in flavonoid synthesis and the flavonoid-mediated drought response mechanism remain elusive. In this study, we demonstrated that a drought-responsive HSF, designated MdHSFA8a, promotes the accumulation of flavonoids, scavenging of reactive oxygen species, and plant survival under drought conditions. A chaperone, HEAT SHOCK PROTEIN90 (HSP90), interacted with MdHSFA8a to inhibit its binding activity and transcriptional activation. However, under drought stress, the MdHSP90-MdHSFA8a complex dissociated and the released MdHSFA8a further interacted with the APETALA2/ETHYLENE RESPONSIVE FACTOR family transcription factor RELATED TO AP2.12 to activate downstream gene activity. In addition, we demonstrated that MdHSFA8a participates in abscisic acid-induced stomatal closure and promotes the expression of abscisic acid signaling-related genes. Collectively, these findings provide insight into the mechanism by which stress-inducible MdHSFA8a modulates flavonoid synthesis to regulate drought tolerance.

摘要

干旱是影响全球农业作物和水果生长和生产的重要环境因素()。热休克因子(HSFs)在应激反应中具有很好的功能记录,但它们在类黄酮合成和类黄酮介导的干旱响应机制中的作用仍不清楚。在这项研究中,我们证明了一个干旱响应的 HSF,命名为 MdHSFA8a,促进类黄酮的积累,清除活性氧,以及植物在干旱条件下的生存。伴侣蛋白,热休克蛋白 90(HSP90)与 MdHSFA8a 相互作用,抑制其结合活性和转录激活。然而,在干旱胁迫下,MdHSP90-MdHSFA8a 复合物解离,释放的 MdHSFA8a 进一步与 APETALA2/ETHYLENE RESPONSIVE FACTOR 家族转录因子 RELATED TO AP2.12 相互作用,激活下游基因活性。此外,我们证明 MdHSFA8a 参与脱落酸诱导的气孔关闭,并促进脱落酸信号相关基因的表达。总之,这些发现为应激诱导的 MdHSFA8a 调节类黄酮合成以调节耐旱性的机制提供了深入了解。

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