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根癌农杆菌通过调节拟南芥中的病原体防御来促进肿瘤的诱导。

Agrobacterium tumefaciens promotes tumor induction by modulating pathogen defense in Arabidopsis thaliana.

机构信息

Julius-von-Sachs-Institute, Department of Molecular Plant Physiology and Biophysics, University of Wuerzburg, Wuerzburg, Germany.

出版信息

Plant Cell. 2009 Sep;21(9):2948-62. doi: 10.1105/tpc.108.064576. Epub 2009 Sep 30.

DOI:10.1105/tpc.108.064576
PMID:19794116
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2768927/
Abstract

Agrobacterium tumefaciens causes crown gall disease by transferring and integrating bacterial DNA (T-DNA) into the plant genome. To examine the physiological changes and adaptations during Agrobacterium-induced tumor development, we compared the profiles of salicylic acid (SA), ethylene (ET), jasmonic acid (JA), and auxin (indole-3-acetic acid [IAA]) with changes in the Arabidopsis thaliana transcriptome. Our data indicate that host responses were much stronger toward the oncogenic strain C58 than to the disarmed strain GV3101 and that auxin acts as a key modulator of the Arabidopsis-Agrobacterium interaction. At initiation of infection, elevated levels of IAA and ET were associated with the induction of host genes involved in IAA, but not ET signaling. After T-DNA integration, SA as well as IAA and ET accumulated, but JA did not. This did not correlate with SA-controlled pathogenesis-related gene expression in the host, although high SA levels in mutant plants prevented tumor development, while low levels promoted it. Our data are consistent with a scenario in which ET and later on SA control virulence of agrobacteria, whereas ET and auxin stimulate neovascularization during tumor formation. We suggest that crosstalk among IAA, ET, and SA balances pathogen defense launched by the host and tumor growth initiated by agrobacteria.

摘要

根癌农杆菌通过将细菌 DNA(T-DNA)转移并整合到植物基因组中来引起冠瘿病。为了研究根癌农杆菌诱导肿瘤发生过程中的生理变化和适应机制,我们比较了拟南芥转录组中水杨酸(SA)、乙烯(ET)、茉莉酸(JA)和生长素(吲哚-3-乙酸 [IAA])的变化。我们的数据表明,宿主对致癌菌株 C58 的反应比对无毒性菌株 GV3101 强烈得多,并且生长素是调控拟南芥-根癌农杆菌互作的关键调节剂。在感染起始时,IAA 和 ET 水平升高与诱导宿主参与 IAA 但不参与 ET 信号的基因有关。在 T-DNA 整合后,SA 以及 IAA 和 ET 积累,但 JA 没有。这与宿主中 SA 控制的与发病相关的基因表达没有相关性,尽管突变体植物中高 SA 水平可防止肿瘤发生,而低水平则促进其发生。我们的数据表明,ET 随后是 SA 控制根癌农杆菌的毒力,而 ET 和生长素则在肿瘤形成过程中刺激新血管生成。我们认为,IAA、ET 和 SA 之间的串扰平衡了宿主发起的病原体防御和根癌农杆菌引发的肿瘤生长。

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