Recycling of Methylthioadenosine Is Essential for Normal Vascular Development and Reproduction in Arabidopsis1[W][OA]

Recycling of Methylthioadenosine Is Essential for Normal Vascular Development and Reproduction in Arabidopsis1[W][OA]
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DOI:
10.1104/pp.111.191072
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发表时间:
2012-02
期刊:
影响因子:
7.4
通讯作者:
Ishari Waduwara-Jayabahu;Yasmin Oppermann;M. Wirtz;Z. T. Hull;S. Schoor;A. Plotnikov;R. Hell;M. Sauter;B. Moffatt
Ishari Waduwara-Jayabahu;Yasmin Oppermann;M. Wirtz;Z. T. Hull;S. Schoor;A. Plotnikov;R. Hell;M. Sauter;B. Moffatt
中科院分区:
生物学1区
文献类型:
--
作者:
Ishari Waduwara-Jayabahu;Yasmin Oppermann;M. Wirtz;Z. T. Hull;S. Schoor;A. Plotnikov;R. Hell;M. Sauter;B. Moffatt

文献摘要

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5‘-甲硫腺苷(MTA)是拟南芥多胺(PA)、烟胺(NA)和乙烯生物合成的常见副产物。MTA的甲硫醇部分被5‘-甲硫基腺苷核苷酶(MTN)回收,生成甲硫代核糖(MTR)和腺嘌呤。MTN双突变体mtn1-1mtn2-1保留了野生型中约14%的MTN酶活性,并表现出包括血管系统改变和生育能力受损的多效性表型。这些异常特征与MTA水平升高、PA谱改变和NA含量降低有关。外源饲喂PAS部分恢复了育性,而补充NA提高了育性,也逆转了脉间黄化。对含有结合MTA的PA合成酶晶体结构的分析表明,相应的酶活性对可用MTA很敏感。表达MTN或人甲硫腺苷磷酸化酶(代谢MTA而不产生MTR)的突变植株出现野生型,证明突变株的异常性状是由于MTA积累而不是MTR降低所致。根据我们的结果,我们认为MTA含量增加影响的关键靶点是真核细胞起始因子5A的温敏胺合成酶活性和亚精胺依赖的翻译后修饰。
5′-Methylthioadenosine (MTA) is the common by-product of polyamine (PA), nicotianamine (NA), and ethylene biosynthesis in Arabidopsis (Arabidopsis thaliana). The methylthiol moiety of MTA is salvaged by 5′-methylthioadenosine nucleosidase (MTN) in a reaction producing methylthioribose (MTR) and adenine. The MTN double mutant, mtn1-1mtn2-1, retains approximately 14% of the MTN enzyme activity present in the wild type and displays a pleiotropic phenotype that includes altered vasculature and impaired fertility. These abnormal traits were associated with increased MTA levels, altered PA profiles, and reduced NA content. Exogenous feeding of PAs partially recovered fertility, whereas NA supplementation improved fertility and also reversed interveinal chlorosis. The analysis of PA synthase crystal structures containing bound MTA suggests that the corresponding enzyme activities are sensitive to available MTA. Mutant plants that expressed either MTN or human methylthioadenosine phosphorylase (which metabolizes MTA without producing MTR) appeared wild type, proving that the abnormal traits of the mutant are due to MTA accumulation rather than reduced MTR. Based on our results, we propose that the key targets affected by increased MTA content are thermospermine synthase activity and spermidine-dependent posttranslational modification of eukaryotic initiation factor 5A.