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证据表明氧化作用会削弱生长素信号转导。

Evidence of oxidative attenuation of auxin signalling.

机构信息

Department of Environmental Science and Technology, University of Maryland, College Park, MD 20742, USA.

出版信息

J Exp Bot. 2013 Jun;64(9):2629-39. doi: 10.1093/jxb/ert152.

DOI:10.1093/jxb/ert152
PMID:23709674
Abstract

Indole-3-acetic acid (IAA) is the principle auxin in Arabidopsis and is synthesized primarily in meristems and nodes. Auxin is transported to distal parts of the plant in response to developmental programming or environmental stimuli to activate cell-specific responses. As with any signalling event, the signal must be attenuated to allow the system to reset. Local auxin accumulations are thus reduced by conjugation or catabolism when downstream responses have reached their optima. In most cell types, localized auxin accumulation increases both reactive oxygen species (ROS) and an irreversible catabolic product 2-oxindole-3-acid acid (oxIAA). oxIAA is inactive and does not induce expression of the auxin-responsive reporters DR5 or 2XD0. Here it is shown that oxIAA is not transported from cell to cell, although it appears to be a substrate for the ATP-binding cassette subfamily G (ABCG) transporters that are positioned primarily on the outer lateral surface of the root epidermis. However, oxIAA and oxIAA-Glc levels are higher in ABCB mutants that accumulate auxin due to defective cellular export. Auxin-induced ROS production appears to be at least partially mediated by the NAD(P)H oxidase RbohD. oxIAA levels are higher in mutants that lack ROS-scavenging flavonoids (tt4) and are lower in mutants that accumulate excess flavonols (tt3). These data suggest a model where IAA signalling is attenuated by IAA catabolism to oxIAA. Flavonoids appear to buffer ROS accumulations that occur with localized increases in IAA. This buffering of IAA oxidation would explain some growth responses observed in flavonoid-deficient mutants that cannot be explained by their established role in partially inhibiting auxin transport.

摘要

吲哚-3-乙酸(IAA)是拟南芥中的主要生长素,主要在分生组织和节中合成。生长素响应发育编程或环境刺激被运输到植物的远端,以激活细胞特异性反应。与任何信号事件一样,信号必须减弱,以使系统重置。当地生长素的积累因此通过共轭或分解代谢来减少,当下游反应达到最佳状态时。在大多数细胞类型中,局部生长素的积累增加活性氧(ROS)和不可逆的分解代谢产物 2-氧吲哚-3-乙酸(oxIAA)。oxIAA 是无活性的,不会诱导生长素响应报告者 DR5 或 2XD0 的表达。这里表明,oxIAA 不能从一个细胞传递到另一个细胞,尽管它似乎是位于根表皮外侧面的主要位置的 ATP 结合盒亚家族 G(ABCG)转运体的底物。然而,oxIAA 和 oxIAA-Glc 水平在由于细胞内输出缺陷而积累生长素的 ABCB 突变体中较高。生长素诱导的 ROS 产生似乎至少部分由 NAD(P)H 氧化酶 RbohD 介导。在缺乏 ROS 清除类黄酮(tt4)的突变体中,oxIAA 水平较高,在积累过量类黄酮(tt3)的突变体中,oxIAA 水平较低。这些数据表明了一个模型,其中生长素信号通过生长素分解代谢为 oxIAA 而减弱。类黄酮似乎缓冲了局部生长素增加时发生的 ROS 积累。这种对生长素氧化的缓冲作用可以解释在缺乏类黄酮的突变体中观察到的一些生长反应,这些反应不能用它们在部分抑制生长素运输中的既定作用来解释。

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