The bacterial cell then elongates and splits into two daughter cells each with identical DNA to the parent cell. Each daughter cell is a clone of the parent cell. When conditions are favourable such as the right temperature and nutrients are available, some bacteria like Escherichia coli can divide every 20 minutes. This means that in just seven hours one bacterium can generate 2,, bacteria.
After one more hour the number of bacteria will have risen to a colossal 16,, Some bacteria can form endospores. These are dormant structures, which are extremely resistant to hostile physical and chemical conditions such as heat, UV radiation and disinfectants.
This makes destroying them very difficult. Many endospore-producing bacteria are nasty pathogens, for example Bacillus anthracis , the cause of anthrax.
Educational resource for students: Observing bacteria cultures in a Petri dish and learning about colony morphology. The organisms that cause tuberculosis in humans and animals, Mycobacterium tuberculosis and Mycobacterium bovis , are featured in this edition of Microbiology Today alongside Mycobacterium leprae , the cause of leprosy, and Mycobacterium ulcerans , which causes Buruli ulcer.
Often, the first things that come to mind when we think about microbes in the built environment are damage, decay, discolouration and staining to building materials and their surfaces. Tuberculosis TB is a debilitating multi-organ disease caused by the bacterium Mycobacterium tuberculosis.
The most important form of the disease is pulmonary TB, an infection of the lungs and respiratory tract. The threat of antimicrobial resistance AMR has now been recognised globally and it is estimated that 10 million people a year will die due to antimicrobial resistance by if no urgent action is taken.
Species within the genus Pseudomonas are amongst the most researched bacteria in the scientific community. Bacteria in this genus are widely used as model organisms in microbial research, and include a range of important species in fields such as plant pathogenicity, bioremediation, and environmental microbiology. While these schemes previously allowed the identification and classification of bacterial strains, it was long unclear whether these differences represented variation between distinct species or between strains of the same species.
This uncertainty resulted from the lack of distinctive structures in most bacteria, as well as lateral gene transfer that occurred between unrelated species. Because of the existence of lateral gene transfer, some closely related bacteria have very different morphologies and metabolisms. To overcome these uncertainties, modern bacterial classification emphasizes molecular systematics, using genetic techniques such as guanine cytosine ratio determination, genome-genome hybridization, as well as sequencing genes that have not undergone extensive lateral gene transfer, such as the rRNA gene.
While there are several molecular tools that allow us to classify or distinguish different bacterial species, this is predicated on obtaining uni-species cultures of a given bacteria. Culture techniques are designed to promote the growth and identify particular bacteria, while restricting the growth of the other bacteria in the sample.
Often these techniques are designed for specific specimens; for example, a sputum sample will be treated to identify organisms that cause pneumonia, while stool specimens are cultured on selective media to identify organisms that cause diarrhoea while preventing growth of non- pathogenic bacteria.
Specimens that are normally sterile, such as blood, urine, or spinal fluid, are cultured under conditions designed to grow all possible organisms. Once a pathogenic organism has been isolated, it can be further characterized by its morphology, by growth patterns such as aerobic or anaerobic growth, by patterns of hemolysis and by staining.
If a bacteria can not be cultured, classification can prove to be very difficult. However, recent advances in molecular techniques do allow the sequencing of DNA from bacterial species, without the reliance on a pure culture of that given bacteria. Diagnostics using such DNA-based tools, such as polymerase chain reaction, are increasingly popular due to their specificity and speed, compared to culture-based methods.
However, even using these improved methods, the total number of bacterial species is not known and cannot even be estimated with any certainty. Following present classification, there are a little less than 9, known species of prokaryotes, which includes bacteria and archaea. Attempts to estimate the true level of bacterial diversity have ranged from 10 7 to 10 9 total species — and even these diverse estimates may be off by many orders of magnitude.
Privacy Policy. Skip to main content. Microbial Evolution, Phylogeny, and Diversity. Focusing on the nucleotide switch at the heart of the motor, these cytoskeletal molecular motors are members of what is called the P-loop NTPase family. There has been a heroic attempt made by Eugene Koonin and colleagues to classify all of these many very divergent proteins into a reasonable phylogenetic tree based on sequence and structural similarities [ 97 ].
Given that this is such a diverse protein family spanning essentially the whole history of cellular evolution, there is some uncertainty here, but one thing about their reconstructed phylogeny really leapt out at me. According to their analysis, there is a entire branch of the P-loop NTPases that is found only in eukaryotes, and not in bacteria or archaea. This branch includes not only myosin and kinesin, but also many other critical proteins that we associate with eukaryotic cellular complexity.
These include the Rho GTPase superfamily, which act as master regulators for actin cytoskeletal assembly [ 98 ], the Rab GTPases that govern many aspects of membraneous organelle identity [ 99 ], the Arf GTPases that are also associated with membrane traffic [ ], the Ran GTPase that governs the directionality of nuclear import and export [ ], and the heterotrimeric G proteins that influence so many aspects of eukaryotic cell-to-cell signaling [ ].
So, wow. This looks very much like the list of eukaryotic-specific cellular features that we started off with. It seems historically as if a branch of the P-loop NTPase family might have arisen in eukaryotes at some point when they had presumably already been evolutionarily separated from the bacteria and the archaea, and this novel protein family gave rise not just to the myosins and kinesins, but also to many of the regulatory and signaling proteins that we most closely associate with the eukaryotic way of life.
Bacteria, of course, have very good signalling proteins, such as the large family of two-component signal transduction systems involving histidine kinases and response regulators [ ]. Who knows why that happened - maybe it was just good luck, maybe the innovation that led to those branches of the P-loop NTPase superfamily is something that happened in eukaryotes so that they were able to seize advantage of it and then combine it with their other properties and develop the ability to make these very large and elaborate, well organized and polarized cytoskeletal structures that would enable them to do things like build a mitotic spindle.
Bacteria already had a perfectly good strategy going without these kinds of systems. Arguably in many ways the prokaryotic side of the tree, the bacteria and archaea, are much more diverse and more successful than eukaryotes - certainly there are many more of them than there are of us.
They are particularly good at diversifying their metabolisms. All of the really exciting inventions in biological chemistry, I would say, have been generated in the prokaryotic branches of the tree.
Photosynthesis, for example, is simply an awesome idea, and it was cyanobacteria that came up with that. Eukaryotes never could come up with that whole crazy business about using a cubic manganese cluster to strip the electrons off of water [ ]. The best that eukaryotes could do was to tame the cyanobacteria and get them to come and live inside and become chloroplasts.
I think the bacterial strategy is terrific, it is just different from our eukaryotic strategy. Our strategy has much more to do with morphological diversification, including getting very large both as cells and as organisms, and developing hunting strategies of various different kinds. I think this is probably both a consequence and a cause in a feedback loop mechanism of the diversification of cytoplasmic cytoskeletal structures that then gave rise to larger-scale morphological diversity in eukaryotes.
This fourth part of my argument is now much more speculative than even the most speculative parts of what I have said before. Let us stipulate that it is observable that all cells are organized in some way. What is their central organizing principle? Where is the information that is used by various different components of the cell to know where they are in relationship to everyone else?
In most bacteria there are only one or a few chromosomes. They tend to be oriented in a very reproducible way as you go from one individual to the next [ , ] and because of the coupled transcription and translation, the physical site where you have a bit of DNA is also connected to the physical site where you make the RNA and the physical site where you make the protein from that bit of information [ ].
If it is important to a bacterial cell to be able to target something to a specific location, it already has all the information it could ever hope for about which location in the cytoplasm is which because it has a well-defined, oriented chromosome present there.
It is a very difficult chicken-and-egg problem as to what came first. Was it the wrapping of the nucleus that caused the actin and tubulin cytoskeletons to expand their capacities, or was it the explosion of the capacity of the cytoskeleton that wrapped up the nucleus in membrane? I like to imagine that at some point the nucleus got sequestered away somehow by some sort of prototypical membrane, maybe like what we see now in Gemmata , and then the poor little cytoskeletal elements were left out there in the cytoplasm on their own.
They had no way of knowing where they were or of measuring space or position. So they had to figure out how to do it by themselves, without the chromosome there to help. Our eukaryotic cytoskeletons figured out how to do this by setting up large-scale arrays that can be oriented by virtue of having nucleators and molecular motor proteins to make those type B structures that are so useful for spatial organization over vast distances of many tens of micrometers. I think that this is a very elegant solution.
The other benefit that the eukaryotes may have gotten from this strategic decision is extra morphological evolvability. In one of your other interviews, Marc Kirschner made some very interesting points about how certain kinds of preexisting conditions may make it relatively easy for some animal lineages to generate highly variable morphology [ ].
I think the eukaryotic cytoskeleton may well be an example of this at the cellular level, an idea that Marc also certainly shares [ ]. Once the lonely but inventive eukaryotic cytoskeletal proteins committed to the strategy of using a very small number of filament types to perform a large number of different functions, the addition of a new kind of organizational function to the underlying cytoskeletal framework may have been as simple as coming up with a few new modulators of cytoskeletal filament dynamics, or another kind of slightly modified motor protein.
This diversification may have happened very quickly on an evolutionary scale. Sequence analysis of the myosin and kinesin motor families seems to suggest that the most recent common ancestor for all the currently living eukaryotes already had several different kinds of each motor [ , ].
Indeed this most recent common ancestor may even have been capable of both amoeboid crawling motion and flagellar swimming [ ]. It may be that the bacteria just never had to face this particular problem because, again, almost universally they have kept their chromosome right there in the cytoplasmic compartment where they could use it for spatial information.
So typically, when a particular bacterium needs to make a filamentous structure for a novel purpose, such as orienting the magnetosomes in Magnetospirillum [ 5 ], it duplicates the gene for a cytoskeletal filament and adapts it for that one new purpose. This works fine for the purpose at hand, but forgoes the opportunity for flexibility and truly large-scale cellular organization that are intrinsic features of both the eukaryotic actin and microtubule cytoskeletons.
Knowing eukaryotes, I would guess that the ones that figured out how to do phagocytosis first just ate everybody else. At some point initially, the earliest eukaryote must have looked much like its contemporary bacterial and archaeal counterparts, but it had secrets inside it that enabled it to become different. I think the fact that you see that both the diversification of the important NTPase families and the elaboration of cytoskeletal functions seem to be universal among eukaryotes means that probably those things happened relatively quickly.
So I suspect the original eukaryote was small. I suspect it was pretty simple-looking compared with Stentor or one of the really fabulous single-celled eukaryotes. PLoS Biol. EMBO J. Raven PH: A multiple origin for plastids and mitochondria. Google Scholar. Cold Spring Harb Perspect Biol.
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BMC Evol Biol. Download references. You can also search for this author in PubMed Google Scholar. Correspondence to Julie A Theriot. This article is published under license to BioMed Central Ltd. Reprints and Permissions. Theriot, J. Why are bacteria different from eukaryotes?. BMC Biol 11, Download citation.
Received : 09 December Accepted : 09 December Published : 13 December Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Julie Theriot. How different are they in fact? So how does that affect the function of bacterial and eukaryotic cells?
Or might evolve Yes, or might evolve. Figure 1. Full size image. This is bacterial cell division? Figure 2. I think it would be good to know all four supporting arguments for your hypothesis. Can we start with number one?
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