n nnnAgrobacterium tumefaciens causes crown gall disease by transferringand integrating bacterial DNA (T-DNA) into the plant genome.To examine the physiological changes and adaptations duringAgrobacterium-induced tumor development, we compared the profilesof salicylic acid (SA), ethylene (ET), jasmonic acid (JA), andauxin (indole-3-acetic acid [IAA]) with changes in the Arabidopsisthaliana transcriptome. Our data indicate that host responseswere much stronger toward the oncogenic strain C58 than to thedisarmed strain GV3101 and that auxin acts as a key modulatorof the Arabidopsis–Agrobacterium interaction. At initiationof infection, elevated levels of IAA and ET were associatedwith the induction of host genes involved in IAA, but not ETsignaling. After T-DNA integration, SA as well as IAA and ETaccumulated, but JA did not. This did not correlate with SA-controlledpathogenesis-related gene expression in the host, although highSA levels in mutant plants prevented tumor development, whilelow levels promoted it. Our data are consistent with a scenarioin which ET and later on SA control virulence of agrobacteria,whereas ET and auxin stimulate neovascularization during tumorformation. We suggest that crosstalk among IAA, ET, and SA balancespathogen defense launched by the host and tumor growth initiatedby agrobacteria.展开▼
机译:ABSTRACTn FONT> TH> TR> TABLE> n
n TOP n <字体颜色= 464c53>抽象 FONT> n 介绍 n 结果 n 讨论 n 结论 n 方法 n 参考资料 n FONT> TH> TR> TABLE> n nnn 根癌农杆菌 I>通过转移 SUP>并整合细菌DNA(T -DNA)进入植物基因组。 SUP>为了检查 SUP> 农杆菌引起的肿瘤发生过程中的生理变化和适应性,我们比较了 SUP>的水杨酸(SA),乙烯(ET),茉莉酸(JA)和 SUP>生长素(吲哚-3-乙酸[IAA])随拟南芥的变化而变化 SUP>拟南芥 I>转录组。我们的数据表明,对致癌菌株C58的宿主应答 SUP>比对 SUP>解除武装的菌株GV3101的应答强得多,并且生长素充当了该菌株的关键调节剂 SUP> 拟南芥 I> – 农杆菌 I>的相互作用。感染开始 SUP>时,IAA和ET的升高水平与诱导参与IAA的宿主基因相关,但与ET SUP>信号无关。在T-DNA整合之后,SA以及IAA和ET SUP>都累积了,而JA则没有。这与宿主中受SA控制的 SUP>致病相关基因的表达无关,尽管突变植物中较高的 SUP> SA水平阻止了肿瘤的发生,而 SUP>低水平促进了它。我们的数据与 SUP>方案一致,在该方案中,ET和后来的SA控制农杆菌的毒力, SUP>,而ET和生长素在肿瘤形成过程中刺激新血管形成。我们建议,IAA,ET和SA平衡之间的串扰 SUP>由宿主启动的病原体防御和肿瘤生长由农杆菌引发的 SUP>。 SUP>
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