INTERACTIONS BETWEEN AGROBACTERIUM AND HOST PLANTS

我们建议研究化学信号的双向交换， 病原微生物根癌农杆菌及其植物宿主。这 一种微生物通过转移一种 将致癌DNA片段插入植物基因组中。我们的主要重点是 基因对化学信号的转录调节 从主机中释放。几乎所有的病原体都会诱导发病机制相关的 响应宿主释放信号的基因，以及A.根瘤菌是一种 这是研究这一现象的重要模型。在感染开始时， 伤口释放的化合物通过三种蛋白质（跨膜蛋白）起作用。 感觉蛋白激酶VirA，反应调节因子VirG，以及 周质糖结合蛋白ChvE）以激活细胞的转录。 vir调节子。后来，一种叫做章鱼碱的化合物通过OccR 蛋白（LysR型蛋白）诱导其他基因，包括 接合调节子TraR。TraR和TraI是LuxR/LuxI的成员 群体感应蛋白家族，并仅在高供体条件下诱导tra基因 细胞密度至少一种其他植物病原体和一种动物病原体 （铜绿假单胞菌）使用同源蛋白质来调节发病机制- 相关基因我们工作的第二个重点是研究T- 与宿主的DNA吻合。我们将确定是否有三个以前 vir区域中的未表征基因是毒力所必需的，并且 是否受VirG监管我们还将研究一个来自 作为virB操纵子的11个基因的模型的不同质粒， 这两个操纵子是紧密同源的。理解这些变化- 类似的过程可能会导致新的方法来防止抗生素的转移， 细菌之间的抗性基因和毒素决定簇。更一般 这种现象是大分子复合物从 细胞和细胞之间的运输这些复合物。

We propose to study the two-way exchange of chemical signals between the pathogenic microbe Agrobacterium tumefaciens and its plant hosts. This organism causes crown gall tumors in higher plants by transferring a segment of oncogenic DNA into the plant genome. Our primary focus is on the transcriptional regulation of genes in response to chemical signals released from hosts. Virtually all pathogens induce pathogenesis-related genes in response to host-released signals, and A. tumefaciens is a valuable model for studying this phenomenon. At the outset of infection, wound-released compounds act through three proteins (the transmembrane sensory protein kinase VirA, the response regulator VirG, and the periplasmic sugar binding protein ChvE) to activate transcription of the vir regulon. Later, a compound called octopine acts through the OccR protein (a LysR-type protein) to induce other genes, including the conjugation regulator TraR. TraR and TraI are members of the LuxR/LuxI family of quorum-sensing proteins, and induce tra genes only at high donor cell densities. At least one other plant pathogen and one animal pathogen (Pseudomonas aeruginosa) use homologous proteins to regulate pathogenesis- related genes. A second focus of our work is to study the transfer of T- DNA to the host. We will determine whether three previously uncharacterized genes in the vir region are required for virulence, and whether they are regulated by VirG. We will also study a tra operon from a different plasmid as a model for the eleven genes of the virB operon, as the two operons are closely homologous. Understanding these conjugation- like processes may lead to new ways to prevent the transfer of antibiotic resistance genes and toxin determinants between bacteria. More generally this phenomenon is an example of export of macromolecular complexes from cells and transport of these complexes between cells.