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拟南芥发育及防御过程中两个同源基因——异常生长与死亡2(aberrant growth and death2)和类AGD2防御反应蛋白1(AGD2-LIKE DEFENSE RESPONSE PROTEIN1)的不同作用,这两个基因编码新型氨基转移酶。

Divergent roles in Arabidopsis thaliana development and defense of two homologous genes, aberrant growth and death2 and AGD2-LIKE DEFENSE RESPONSE PROTEIN1, encoding novel aminotransferases.

作者信息

Song Jong Tae, Lu Hua, Greenberg Jean T

机构信息

Department of Molecular Genetics and Cell Biology, University of Chicago, Chicago, Illinois 60637.

出版信息

Plant Cell. 2004 Feb;16(2):353-66. doi: 10.1105/tpc.019372. Epub 2004 Jan 16.

DOI:10.1105/tpc.019372
PMID:14729919
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC341909/
Abstract

The disease-resistant Arabidopsis thaliana aberrant growth and death2 (agd2-1) mutant has elevated levels of the defense signal salicylic acid (SA), altered leaf morphology, and mild dwarfism. AGD2 and its close homolog ALD1 (for AGD2-LIKE DEFENSE RESPONSE PROTEIN1) encode aminotransferases that act on an overlapping set of amino acids in vitro. However, kinetic parameters indicate that AGD2 and ALD1 may drive the aminotransferase reaction in opposite directions. ALD1-deficient mutants have the opposite phenotypes from agd2-1, showing reduced SA production and increased disease susceptibility. Furthermore, ALD1 transcript levels are elevated in agd2-1 and are induced in the wild type by bacterial pathogen infection. ALD1 is responsible for some of the elevated SA content and a majority of the disease resistance and dwarfism of agd2-1. A complete knockout of AGD2 renders embryos inviable. We suggest that AGD2 synthesizes an important amino acid-derived molecule that promotes development and suppresses defenses, whereas ALD1 generates a related amino acid-derived molecule important for activating defense signaling.

摘要

抗病性拟南芥异常生长与死亡2(agd2-1)突变体中防御信号水杨酸(SA)水平升高,叶片形态改变,且有轻度矮化现象。AGD2及其紧密同源物ALD1(类AGD2防御反应蛋白1)编码的氨基转移酶在体外作用于一组重叠的氨基酸。然而,动力学参数表明AGD2和ALD1可能驱动氨基转移酶反应朝相反方向进行。ALD1缺陷型突变体具有与agd2-1相反的表型,表现出SA产生减少和疾病易感性增加。此外,agd2-1中ALD1转录水平升高,并且在野生型中受细菌病原体感染诱导。ALD1导致了agd2-1中部分SA含量升高以及大部分抗病性和矮化现象。AGD2的完全敲除会使胚胎无法存活。我们认为AGD2合成一种促进发育并抑制防御的重要氨基酸衍生分子,而ALD1产生一种对激活防御信号很重要的相关氨基酸衍生分子。

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