Mechanisms of host-parasite interactions between bacteriophages and Erwinia amylovora

微生物多样性和细菌在生态系统功能中的作用受到噬菌体相互作用的极大影响。这些相互作用可能很复杂，但最基本的是单个噬菌体在单个细菌中攻击和繁殖的能力。这种能力是由细菌基因组编码的成分，如表面受体和几种防御系统，并通过噬菌体基因组。拟议的研究涉及研究攻击细菌物种欧文氏菌和成团泛菌的噬菌体的基因，以促进宿主致病。我们最近对十九种噬菌体的基因组进行了测序，这些噬菌体在与几种宿主物种的相互作用中是单独可变的。观察了噬菌体与E.食淀粉菌的致病性包括具有后代产生的裂解，其变化超过四个数量级，溶原性和假溶原性，或没有任何明显的攻击。这些序列信息对于理解噬菌体攻击中所有这些变异的遗传控制是一个有价值的资源。本研究的具体短期目标包括：（1）噬菌体基因与宿主攻击变异的相关性和这些基因的注释;（2）噬菌体通过特定细菌宿主重复传代的共进化实验，以寻找/选择改变的相互作用，并观察（1）中鉴定的基因中的任何突变变化;和（3）在噬菌体中人工诱导突变，导致与宿主的相互作用改变，并将这些突变与（1）中鉴定的基因相关联。长期目标将包括宿主编码的属性与这些噬菌体组分的相关性。拟议研究的预期意义在于，我们将确定噬菌体攻击的各种分子机制，并最终确定所有这些观察到的变化如何影响微生物多样性和种群动态。

Microbial diversity and the roles of bacteria in the function of ecosystems are greatly influenced by interactions with bacteriophages. These interactions can be complex but at the most basic level is the ability of an individual bacteriophage to attack and multiply within a single bacterium. This ability is determined by the bacterial genome encoding components such as surface receptors and several defense systems, and by the bacteriophage genome. The proposed research involves investigation of the genes of bacteriophages that attack the bacterial species, Erwinia amylovora and Pantoea agglomerans, for contributions to host pathogenesis. We have recently sequenced the genomes of nineteen bacteriophages that are individually variable in interaction with several host species. Observed interactions between the bacteriophages and E. amylovora include lysis with progeny production that varies over four orders of magnitude, lysogeny, and pseudolysogeny, or no apparent attack whatsoever. This sequence information is a valuable resource for understanding the genetic control of all of this variation in bacteriophage attack. Specific short term objectives of this research will involve: (1) correlation of bacteriophage genes with variation in host attack and annotation of these genes; (2) co-evolution experiments with repeated passages of the bacteriophages through a specific bacterial host to look/select for altered interaction and to observe any mutational changes in the genes identified in (1); and, (3) to artificially induce mutations in bacteriophages that result in altered interaction with the host and to relate these mutations to the genes identified in (1). Long term objectives will include correlation of host-encoded attributes with these bacteriophage components. The expected significance of the proposed research is that we shall identify various molecular mechanisms of bacteriophage attack and ultimately how all of this observed variation impacts on microbial diversity and population dynamics.