REVERSAL OF RDO5 1, a Homolog of Rice Seed Dormancy4, Interacts with bHLH57 and Controls ABA Biosynthesis and Seed Dormancy in Arabidopsis
REVERSAL OF RDO5 1, a Homolog of Rice Seed Dormancy4, Interacts with bHLH57 and Controls ABA Biosynthesis and Seed Dormancy in Arabidopsis
复制标题
水稻种子休眠同源物 RDO5 1 的逆转与 bHLH57 相互作用并控制拟南芥中的 ABA 生物合成和种子休眠
DOI：
10.1105/tpc.20.00026
复制
发表时间：
2020-06-01
期刊：
影响因子：
11.6
通讯作者：
Xiang, Yong
中科院分区：
文献类型：
--
作者：
Liu, Fei;Zhang, Hui;Xiang, Yong
ODR1通过与转录因子bHLH57相互作用，阻止其诱导NCED6和NCED9的表达和ABA的生物合成，从而负向控制种子休眠。脱落酸(ABA)对种子休眠的控制已经得到了广泛的研究，但其内在机制还不完全清楚。在这里，我们报道了两个与ABA相关的拟南芥种子休眠调节因子的特征：ODR1(逆转rdo5)，水稻种子dormancy4的同源基因(Sdr4)和碱性螺旋-环-螺旋转录因子bHLH57。ODR1的转录水平直接被转录因子ABA INSENSITIVE3(ABI3)抑制，它通过影响ABA的生物合成和ABA信号转导来负向调节种子休眠。相反，bHLH57通过诱导编码ABA生物合成酶的基因9-CIS-EPOXYCAROTENOID DIOXYGENASE(NCED6)和NCED9的表达来正向调节种子休眠，从而导致较高的ABA水平。ODR1与bHLH57相互作用，并抑制bHLH57调控的NCED6和NCED9在细胞核内的表达。Bhlh57功能缺失等位基因可以部分抵消odr1突变体中增强的NCED6和NCED9的表达，从而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，该网络为研究ABA生物合成和信号转导对种子休眠的调控提供了深入的信息。
ODR1 negatively controls seed dormancy by interacting with the transcription factor bHLH57 and preventing its induction of NCED6 and NCED9 expression and ABA biosynthesis. 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 (Arabidopsis thaliana): ODR1 (for reversal of rdo5), an ortholog of the rice (Oryza sativa) Seed dormancy4 (Sdr4), and the basic helix-loop-helix transcription factor bHLH57. ODR1, 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 9-CIS-EPOXYCAROTENOID DIOXYGENASE6 (NCED6) and NCED9, which encode ABA biosynthetic enzymes, and thus leads to higher ABA levels. ODR1 interacts with bHLH57 and inhibits bHLH57-modulated NCED6 and NCED9 expression in the nucleus. bhlh57 loss-of-function alleles can partially counteract the enhanced NCED6 and NCED9 expression seen in odr1 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.