Liu Gui-Rong, Rahn Andrea, Liu Wei-Qiao, Sanderson Kenneth E, Johnston Randal N, Liu Shu-Lin
Department of Microbiology and Infectious Diseases, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N1, Canada.
J Bacteriol. 2002 May;184(10):2626-33. doi: 10.1128/JB.184.10.2626-2633.2002.
Salmonella enterica serovar Pullorum is a fowl-adapted bacterial pathogen that causes dysentery (pullorum disease). Host adaptation and special pathogenesis make S. enterica serovar Pullorum an exceptionally good system for studies of bacterial evolution and speciation, especially regarding pathogen-host interactions and the acquisition of pathogenicity. We constructed a genome map of S. enterica serovar Pullorum RKS5078, using I-CeuI, XbaI, AvrII, and SpeI and Tn10 insertions. Pulsed-field gel electrophoresis was employed to separate the large DNA fragments generated by the endonucleases. The genome is 4,930 kb, which is similar to most salmonellas. However, the genome of S. enterica serovar Pullorum RKS5078 is organized very differently from the majority of salmonellas, with three major inversions and one translocation. This extraordinary genome structure was seen in most S. enterica serovar Pullorum strains examined, with different structures in a minority of S. enterica serovar Pullorum strains. We describe the coexistence of different genome structures among the same bacteria as genomic plasticity. Through comparisons with S. enterica serovar Typhimurium, we resolved seven putative insertions and eight deletions ranging in size from 12 to 157 kb. The genomic plasticity seen among S. enterica serovar Pullorum strains supported our hypothesis about its association with bacterial evolution: a large genomic insertion (157 kb in this case) disrupted the genomic balance, and rebalancing by independent recombination events in individual lineages resulted in diverse genome structures. As far as the structural plasticity exists, the S. enterica serovar Pullorum genome will continue evolving to reach a further streamlined and balanced structure.
鸡白痢沙门氏菌是一种适应家禽的细菌病原体，可引起痢疾（鸡白痢病）。宿主适应性和特殊的发病机制使鸡白痢沙门氏菌成为研究细菌进化和物种形成的绝佳系统，特别是在病原体与宿主相互作用以及致病性获得方面。我们使用I-CeuI、XbaI、AvrII、SpeI和Tn10插入构建了鸡白痢沙门氏菌RKS5078的基因组图谱。采用脉冲场凝胶电泳分离内切酶产生的大DNA片段。该基因组为4930 kb，与大多数沙门氏菌相似。然而，鸡白痢沙门氏菌RKS5078的基因组组织与大多数沙门氏菌非常不同，有三个主要倒位和一个易位。在大多数检测的鸡白痢沙门氏菌菌株中都观察到这种特殊的基因组结构，少数鸡白痢沙门氏菌菌株具有不同的结构。我们将同一细菌中不同基因组结构的共存描述为基因组可塑性。通过与鼠伤寒沙门氏菌进行比较，我们确定了7个推定插入和8个缺失，大小从12到157 kb不等。鸡白痢沙门氏菌菌株中观察到的基因组可塑性支持了我们关于其与细菌进化关联的假设：一个大的基因组插入（在这种情况下为157 kb）破坏了基因组平衡，各个谱系中通过独立重组事件进行的重新平衡导致了不同的基因组结构。只要结构可塑性存在，鸡白痢沙门氏菌基因组将继续进化以达到更简化和平衡的结构。
