Insights from Plague Genomics, Part 1: The Chromosome

Most of the news lately has been about the plague phylogenetic tree produced by looking at single nucleotide polymorphisms (SNPs). The plague tree is remarkably simple and can lead to the mistaken impression that the rest of plague genomics are/will be simple. Michel Drancourt has recently compiled an array of genomic information that shows that SNPs are only part of the story.

A more broad view of plague genomics illustrates why the four biovars will continue to be used in scientific and clinical work. The four biovars are easily distinguished by their phenotype (traits that you can see or measure), the most common and easiest way for plague to be typed in clinical settings. It is important to note that the biovars/phenotypes tell clinicians most of what they need to know to treat the patient(s), their only real goal. Naturally, the biovars reflect genomic clusters beyond the metabolic skills measured in the standard phenotype.

Table and figure from Drancourt, 2012.

Chromosomal rearrangements have been the primary evolutionary mechanism of Yersinia pestis. The figure above shows clones representing the four biovars illustrating rearrangements (follow the lines) and inversions (shown underneath the center line representing each clone’s chromosome). These rearrangements are important for two reasons. First, this is a primary mechanism for DNA loss. Recombination errors can cause  sections of the chromosome to be lost. If the section does not contain vital genes, it will make the clone a leaner specialist. This makes sense of the 13% of parental Yersinia pseudotuberculosis genome lost by Y. pestis, while only gaining two coding sequences among eight new loci. Therefore, other Y. pestis specific genes are all contained on plasmids or other mobile elements.   Second, gene rearrangements can change control of gene expression. Although bacteria do not control their genes individually like eukaryotes, they are controlled in sets called operons. Presumably, genomic rearrangements, that do not respect gene or operon  structure, could change the gene compliment of an operon or destroy the operon control regions deregulating its genes. It can also destroy gene function resulting in pseudogenes (relics or wrecks of former genes). Natural selection will eliminate any damaging rearrangements and favor rearrangements that enhance efficient control. Natural selection works so well on operons that they often contain only genes related to specific metabolic pathways and functions.

Genomic rearrangements continue today. The North American strains provide a datable short-range evolutionary history. In only about 100 years the North American clones have gained one genome rearrangement, six inversions, and several SNPs. Despite all the rearrangements shown in the figure above and the loss of Y. pseudotuberculosis sequences, sequenced clones from all the biovars represented above have similar sized genomes. With the current set of hosts, this suggests that the genome is pared down to near its optimal size. For all the little extras that make Y. pestis an effective pathogen, the plasmids take center stage, and I’ll cover those in part 2.

Drancourt, M (2012). Plague in the genomic era Clinical Microbiology and Infection, 18, 224-230

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