There is a myth about clonal reproduction that says the clones are all the same, except for the inevitable handful of mutations that accompany any reproduction event. When I started preparing this post, I was aware this idea had been shown false in the 1970's. I learned something during my research.
Escherichia coli is a clonal species. The best-understood components of its clonal variation are the flagellar (H) and polysaccharide (O) antigens, both well documented since the mid-1930s because of their use in serotyping.
Some of the mechanisms of clonal variation have been studied, naturally, but investigation is continuing. Research in this field is really only beginning. Clonal variation is not some oddball exception, either. Anywhere clonal reproduction is found, you'll find it.
The myth relies on the misconception that lifeforms only carry a single blueprint. In reality, plans for variations of many parts are always present. We know that variety is good for life, and even "clonal" lifeforms possess toolkits for producing it.
The Escherichia coli phosphate (PHO) regulon includes 31 (or more) genes arranged in eight separate operons. All are coregulated by environmental (extra-cellular) phosphate and are probably involved in phosphorus assimilation. Pi control of these genes requires the sensor PhoR, the response regulator PhoB, the binding protein-dependent Pi-specific transporter Pst, and the accessory protein PhoU. During Pi limitation, PhoR turns on genes of the PHO regulon by phosphorylating PhoB that in turn activates transcription by binding to promoters that share an 18-base consensus PHO Box. When Pi is in excess, PhoR, Pst, and PhoU together turn off the PHO regulon, presumably by dephosphorylating PhoB. In addition, two Pi-independent controls that may be forms of cross regulation turn on the PHO regulon in the absence of PhoR. The sensor CreC, formerly called PhoM, phosphorylates PhoB in response to some (unknown) catabolite, while acetyl phosphate may directly phosphorylate PhoB. Cross regulation of the PHO regulon by CreC and acetyl phosphate may be examples of underlying control mechanisms important for the general (global) control of cell growth and metabolism. © 1993 Wiley-Liss, Inc.
Variation in "clonal" worms:
The worm Caenorhabditis elegans has historically been used as a powerful model to study organismal aging. After a brief reproductive period, an adult worm consists of 959 post-mitotic cells. Telomeres, the natural ends of linear chromosomes, have long been implicated in the aging process of mitotic cells, and telomere shortening has been proposed to be a limiting factor in cell division. The authors show that telomere length of C. elegans chromosomes is independent of organismal aging. Worm telomeres were characterized in detail, and found to vary considerably in individual clones. These differences were conserved over several populations, suggesting that telomere length is controlled by similar mechanisms in worms and mammals, emphasizing the value of C. elegans as a model for telomere biology. However, telomere length has not been found to determine the potential life span of the animals, since worms with short telomeres lived as long as worms with long telomeres.
http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.0010030
In Tobacco
Sister clones isolated from the same cloned line of crown-gall cells obtained by transformation with the pTiT37 plasmid showed an up to eight-fold difference in their ZR and IPA content (30–230 and 21–77 pmol/g fresh weight, respectively). This variation could not be accounted for by differences in the time course of cytokinin accumulation.
In the germs that attack our mouths
Periodontal disease is an infectious disorder caused by a small subset of periodontal pathogens including Porphyromonas gingivalis. Accumulated evidences show that the expression of P. gingivalis heterogenic virulence properties is dependent on its clonal diversity.
Defenders of the myth frequently resort to redefining 'mutation'. This merely concedes defeat. If one equivocates and classifies all adaptation as "mutation", doing so does not even defend the notion that all this variety is the result of random mistakes. Such a "defense" does not deny the work of adaptive mechanisms; it simply tries to steal credit for their work.
They may try to let on that all this variety should have been detected, and thoroughly documented by now. This is just a play on ignorance. We don't live in a sci-fi realm, where a cell can be inserted into a machine, and the machine will generate a full report on every detail about its composition.
Although many strain typing methods exist for pathogenic Escherichia coli, most have drawbacks in terms of resolving power, interpretability, or scalability. For this reason, multilocus sequence typing (MLST) is an appealing alternative. However, its applicability to different pathogens in specific epidemiologic contexts is not well understood.
One has to actively search in order to find most of these things out, and the search is not easy, even with 21st century gadgetry.
It even appears that clonal cells doing what they do, changing from one generation to the next, is an inconvenient for some researchers.
We have developed an E.coli strain with a non-reverting allele of pyrF that is also suitable for cloning.
Next time someone presents a wonderful study claiming they "evolved a clonal lifeform", take a few minutes and fire up your search engine. Enter the name of the lifeform, and "clonal variation". You probably won't have the time or the inclination to read all the results.
