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RDO5 1 的逆转,一种水稻种子休眠 4 的同源物,与 bHLH57 相互作用,控制拟南芥中的 ABA 生物合成和种子休眠。

REVERSAL OF RDO5 1, a Homolog of Rice Seed Dormancy4, Interacts with bHLH57 and Controls ABA Biosynthesis and Seed Dormancy in Arabidopsis.

机构信息

Shenzhen Branch, Guangdong Laboratory for Lingnan Modern Agriculture, Genome Analysis Laboratory of the Ministry of Agriculture, Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences, Shenzhen, China.

Rijk Zwaan, De Lier 2678 ZG, The Netherlands.

出版信息

Plant Cell. 2020 Jun;32(6):1933-1948. doi: 10.1105/tpc.20.00026. Epub 2020 Mar 25.

Abstract

The control of seed dormancy by abscisic acid (ABA) has been extensively studied, but the underlying mechanism is not fully understood. Here, we report the characterization of two ABA-related seed dormancy regulators in Arabidopsis (): ODR1 (for reversal of ), an ortholog of the rice () Seed dormancy4 (Sdr4), and the basic helix-loop-helix transcription factor bHLH57. , whose transcript levels are directly suppressed by the transcription factor ABA INSENSITIVE3 (ABI3), negatively regulates seed dormancy by affecting ABA biosynthesis and ABA signaling. By contrast, bHLH57 positively regulates seed dormancy by inducing the expression of the genes () and , which encode ABA biosynthetic enzymes, and thus leads to higher ABA levels. ODR1 interacts with bHLH57 and inhibits bHLH57-modulated and expression in the nucleus. loss-of-function alleles can partially counteract the enhanced and expression seen in mutants and can therefore rescue their associated hyper-dormancy phenotype. Thus, we identified a novel ABI3-ODR1-bHLH57-NCED6/9 network that provides insights into the regulation of seed dormancy by ABA biosynthesis and signaling.

摘要

脱落酸(ABA)对种子休眠的控制作用已得到广泛研究,但其中的作用机制尚未完全阐明。在此,我们报告了拟南芥中两个与 ABA 相关的种子休眠调控因子的特性:ODR1(代表),是水稻种子休眠 4 号(Sdr4)的同源基因;以及碱性螺旋-环-螺旋转录因子 bHLH57。ABI3(ABA 不敏感 3)的转录因子直接抑制其转录本水平,通过影响 ABA 生物合成和 ABA 信号转导负调控种子休眠。相比之下,bHLH57 通过诱导 ABA 生物合成酶基因()和 的表达来正向调控种子休眠,从而导致 ABA 水平升高。ODR1 与 bHLH57 相互作用,并在核内抑制 bHLH57 调节的和的表达。ODR1 功能丧失突变体可部分抵消 bHLH57 突变体中观察到的和的表达增强,并因此可挽救其相关的超休眠表型。因此,我们鉴定了一个新的 ABI3-ODR1-bHLH57-NCED6/9 网络,该网络为 ABA 生物合成和信号转导调控种子休眠提供了新的见解。

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