This is another archival repost originally written for the old blog in april 2007.
Bacteria tend to get ignored to some extent by writers of popular science and science blogs, except in the context of disease and medicine. There is a general assumption that, as single celled organisms, they must be simple and boring. This extends to secondary science curricula, where one learns of the complicated internal structure of the eukaryotic cell, its biochemical pathways, and interactions with other organisms, and could be forgiven for coming away with the impression that bacteria have none of these properties. On the other hand, one is taught the properties that apply to all life – even though in many cases, bacteria do not fit the model. One such case that came to mind recently, while doing some bacterial comparative genomics, is the concept of the species.
Plant and animal pathogenic bacteria cause disease by entering the spaces between host cells, where they multiply and subsequently attach to the surfaces of the host cells to inject toxins (“effectors”) which disrupt metabolism. The mechanisms by which this occurs are classified as “secretion systems” – complicated collections of proteins that build some impressive needles on the bacteria’s surface. (Those interested in the Intelligent Design issue may be familiar with one such system, the type III secretion system, which is homologous with flagella.[1]) Throughout all this, it must evade or repress the defence systems with which evolution has equipped the hosts.[2]
As a cell surface structure with the specific role of attaching to host cells, the type III secretion system (T3SS) is known to be “hypervariable” – in closely related strains, the genes (and thus proteins) that build the T3SS tend to vary much more than genes which do not have a role in pathogenesis.[3][4] Similarly, great variation is found in genes for constructing efflux pumps, which remove from the bacterial cell substances toxic to it – like the host’s defences, or antibiotic drugs, which are themselves correspondingly diverse.[5] This variation can in part be attributed to evolutionary arms races between the bacteria and their hosts– as the host evolves better T3SS detectors and antibacterial toxins, the bacterium modifies its T3SS and efflux pumps.
However, the variation between strains can not be explained by arms races alone,[6] and a number of observations lead us to another culprit. In the age of genome projects it has become possible to compare the entire genomes of multiple species/strains of bacteria with varying distance of relatedness.[7] When this is done, the strains can be aligned by relatedness. One will find trends of a gene being present in a group of closely related strains, and absent in all of the more distantly related strains – a finding common sense would prepare you for. But one will also find clusters of virulence genes in strains that they shouldn’t be in. Similarly, when analysing newly sequenced genomes, virulence genes are often found that are only found elsewhere in very distantly related species.[8] The reason this occurs is due to horizontal transfer of genes between individuals. This mechanism is quite often ignored in discussions of reproduction and evolution, but is very important – it is why, for example, we have multidrug resistant “super bugs” in hospitals.
In organisms which reproduce asexually, variation is produced by mutation, with both beneficial and harmful mutations accumulating in a cell line. Many eukaryotic organisms have solved the problem of weeding out the harmful ones while preserving the beneficial ones by reproducing sexually – a process that shuffles genes. Bacteria have found another solution. Genes cluster in genomic islands which a bacterium can copy and share, usually with closely related species, by direct contact (“conjugation”). DNA is transferred between more distantly related individuals too, though, for example via viruses. Virulence genes in particular, for example those of the T3SS, have been found on genomic islands known as pathogenicity islands (PAIs).[9]
What does this mean for the species concept? The concept of the species as a static and discrete body has suffered many blows already, starting with the discovery of evolution and its mechanisms. When it became clear that species were continuous, via dead intermediates, and there could be no definitive version of a species, a new paradigm took over. This paradigm saw life as a branching tree, with extant species budding at the end of twigs. But because of extensive horizontal transfer, bacterial species may lie at the end of several fused branches, and it is often difficult to decide how to classify them. However, with horizontal transfer now reported to occur in and between bacteria, some protists, yeast,[10] plants, [11] and perhaps throughout life, the species is looking less stable every day, and perhaps bacteria will turn out not to be so different after all.
References
- ^ Pallen, M.J. and N.J. Matzke. 2006. From The Origin of Species to the origin of bacterial flagella. Nature Reviews Microbiology 4:784-790 Abstract
- ^ Hirano, S.S. and C.D. Upper. 2000. Bacteria in the leaf ecosystem with emphasis on Pseudomonas syringae—a pathogen, ice nucleus, and epiphyte. Microbiol. Mol. Biol. Rev. 64:624-653.
- ^ He, S.Y., and Q. Jin. 2003. The Hrp pilus: learning from flagella. Current Opinion in Microbiology, 6:15-19.
- ^ Alfano, J.R., and A. Collmer. 2004. Type III secretion system effector proteins: Double agents in bacterial disease and plant defence. Annu. Rev. Phytopathol. 42:385-414.
- ^ Piddock, L.J. 2006. Multidrug-resistance efflux pumps – not just for resistance. Nature Rev Microbiol 4:629-36.
- ^ Sarkar S.F., and D.S. Guttman. 2004. Evolution of the core genome of Pseudomonas syringae, a highly clonal, endemic plant pathogen. Appl Environ Microbiol 70:1999-2012.
- ^ And at the Scottish Crop Research Institute in Dundee, they’re making “art” out of it: http://www.dundee.ac.uk/adaeps/shemiltarticle/index.htm
- ^ Joarder, V., M. Lindeberg, R.W. Jackson, J. Selengut, R. Dodson, L.M. Brinkac, S.C. Daugherty, R. DeBoy, A.S. Durkin, M.G. Giglio, R. Madupu, W.C. Nelson, M.J. Rosovitz, S. Sullivan, J. Crabtree, T. Creasy, T. Davidsen, D.H. Haft, N. Zafar, L. Zhou, R. Halpin, T. Holley, H. Khouri, T. Feldblyum, O. White, C.M. Fraser, A.K. Chatterjee, S. Cortinhour, D.J. Schneider, J. Mansfield, A. Collmer and C.R. Buell. 2005. Whole-Genome Sequence Analysis of Pseudomonas syringae pv. phaseolicola 1448A Reveals Divergence among Pathovars in Genes Involved in Virulence and Transposition. Journal of Bacteriology 187:6488–6498
- ^ Summers, A.O. 2006. Genetic linkage and horizontal gene transfer, the roots of the antibiotic multi-resistance problem. Anim Biotechnol 17:125-35.
- ^ Hall C., S. Brachat, and F.S. Dietrich. 2005. Contribution of horizontal gene transfer to the evolution of Saccharomyces cerevisiae. Eukaryot Cell. 4:1102-15
- ^ Richardson, A.O. and J.D. Palmer. 2007. Horizontal Gene Transfer in Plants. Journal of Experimental Botany 58:1-9