首页> 外文期刊>BMC Plant Biology >MYB transcription factor PdMYB118 directly interacts with bHLH transcription factor PdTT8 to regulate wound-induced anthocyanin biosynthesis in poplar
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MYB transcription factor PdMYB118 directly interacts with bHLH transcription factor PdTT8 to regulate wound-induced anthocyanin biosynthesis in poplar

机译:MYB转录因子PDMYB118直接与BHLH转录因子PDTT8相互作用以调节杨树的伤口诱导的花青素生物合成

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R2R3-MYB transcription factors (TFs) play important roles in plant growth and development, and response to biotic and abiotic stresses. However, their regulatory mechanisms in wound-induced anthocyanin biosynthesis in woody plants are largely unknown. In this work, we report that expression of anthocyanin biosynthesis genes (ABGs) were activated by PdMYB118, a MYB TF encoding gene from Populus deltoids, and the activation of PdMYB118 was significantly enhanced by PdTT8, a bHLH protein, through its direct interaction with PdMYB118. PdMYB118 and some ABGs were evidently induced by wound induction and methyl jasmonate (MeJA) treatment. Overexpression of PdMYB118 promoted anthocyanin accumulation in transgenic poplar upon wound induction. Furthermore, a poplar JASMONATE ZIM-domain (JAZ) protein, PtrJAZ1, repressed the transcriptional function of PdMYB118/PdTT8 complex by binding to PdTT8, and wound stimulated the biosynthesis of jasmonic acid (JA) and the degradation of PtrJAZ1. Based on these observations, we proposed that PtrJAZ1 degradation triggered the expression of ABGs, leading to increased biosynthesis of anthocyanins in the wounded leaves of transgenic poplar. Therefore, our findings not only illustrate the crucial role of PdMYB118 in wound-induced anthocyanin biosynthesis in poplar, but also provide a molecular basis for the genetic engineering of colorful tree species.
机译:R2R3-MYB转录因子(TFS)在植物生长和发展中起重要作用,并对生物和非生物应激的反应。然而,他们在木质植物中伤口诱导的花青素生物合成中的调节机制在很大程度上是未知的。在这项工作中,我们报告说,通过PDMYB118,通过与PDMYB118的直接相互作用,PDMYB118通过PDMYB118激活花青素生物合成基因(ABGs)的表达,通过其直接相互作用,通过与PDMYB118的直接相互作用显着增强了PDMYB118的PDMYB118 .PDMYB118的激活。 PDMYB118和一些ABG显然是由伤口诱导和茉莉酸甲酯(MEJA)治疗诱导的。 PDMYB118的过表达促进了伤口诱导转基因杨树中的花青素积累。此外,通过结合PDTT8,杨树茉满红域(Jaz)蛋白,ptrjaz1,压制Pdmyb118 / pdtt8复合物的转录功能,并造成茉莉酸(Ja)的生物合成和ptrjaz1的降解。基于这些观察结果,我们提出了ptrjaz1降解引发了ABG的表达,导致转基因杨树的受伤叶片中的花青素生物合成增加。因此,我们的研究结果不仅说明了PDMYB118在杨树的伤口诱导的花青素生物合成中的关键作用,而且还为彩色树种的基因工程提供了分子基础。

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