Someserotypes, such asEPEC andETEC, are pathogenic, causing seriousfood poisoning in their hosts.[11]Fecal–oral transmission is the major route through which pathogenic strains of the bacterium cause disease. This transmission method is occasionally responsible forfood contamination incidents that prompt product recalls.[12] Cells are able to survive outside the body for a limited amount of time, which makes them potentialindicator organisms to test environmental samples forfecal contamination.[13][14] A growing body of research, though, has examined environmentally persistentE. coli which can survive for many days and grow outside a host.[15]
The bacterium can begrown and cultured easily and inexpensively in a laboratory setting, and has been intensively investigated for over 60 years.E. coli is achemoheterotroph whose chemically defined medium must include a source ofcarbon andenergy.[16]E. coli is the most widely studiedprokaryoticmodel organism, and an important species in the fields ofbiotechnology andmicrobiology, where it has served as thehost organism for the majority of work withrecombinant DNA. Under favourable conditions, it takes as little as 20 minutes to reproduce.[17]
E. coli stains gram-negative because itscell wall is composed of a thinpeptidoglycan layer and anouter membrane. During the staining process,E. coli picks up the color of the counterstainsafranin and stains pink. The outer membrane surrounding the cell wall provides a barrier to certainantibiotics, such thatE. coli is not damaged bypenicillin.[16]
In addition,E. coli's metabolism can be rewired to solely useCO2 as the source ofcarbon for biomass production. In other words, this obligate heterotroph's metabolism can be altered to display autotrophic capabilities by heterologously expressingcarbon fixation genes as well asformate dehydrogenase and conducting laboratory evolution experiments. This may be done by usingformate to reduceelectron carriers and supply theATP required in anabolic pathways inside of these synthetic autotrophs.[25]
Redistribution of fluxes between the three primary glucose catabolic pathways: EMPP (red), EDP (blue), and OPPP (orange) via the knockout of pfkA and overexpression of EDP genes (edd and eda).
E. coli has three native glycolytic pathways:EMPP,EDP, andOPPP. The EMPP employs ten enzymatic steps to yield twopyruvates, twoATP, and twoNADH perglucose molecule while OPPP serves as an oxidation route forNADPH synthesis. Although the EDP is the more thermodynamically favourable of the three pathways,E. coli do not use the EDP forglucose metabolism, relying mainly on the EMPP and the OPPP. The EDP mainly remains inactive except for during growth withgluconate.[26]
Catabolite repression
When growing in the presence of a mixture of sugars, bacteria will often consume the sugars sequentially through a process known ascatabolite repression. By repressing the expression of the genes involved in metabolizing the less preferred sugars, cells will usually first consume the sugar yielding the highest growth rate, followed by the sugar yielding the next highest growth rate, and so on. In doing so the cells ensure that their limited metabolic resources are being used to maximize the rate of growth. The well-used example of this withE. coli involves the growth of the bacterium onglucose andlactose, whereE. coli will consumeglucose beforelactose. Catabolite repression has also been observed inE. coli in the presence of other non-glucose sugars, such asarabinose andxylose,sorbitol,rhamnose, andribose. InE. coli, glucose catabolite repression is regulated by thephosphotransferase system, a multi-proteinphosphorylation cascade that couplesglucose uptake andmetabolism.[27]
The bacterial cell cycle is divided into three stages. The B period occurs between the completion of cell division and the beginning ofDNA replication. The C period encompasses the time it takes to replicate thechromosomal DNA. The D period refers to the stage between the conclusion ofDNA replication and the end of cell division.[30] The doubling rate ofE. coli is higher when more nutrients are available. However, the length of the C and D periods do not change, even when the doubling time becomes less than the sum of the C and D periods. At the fastest growth rates, replication begins before the previous round of replication has completed, resulting in multiple replication forks along theDNA and overlapping cell cycles.[31]
The number of replication forks in fast growingE. coli typically follows 2n (n = 1, 2 or 3). This only happens ifreplication is initiated simultaneously from allorigins of replications, and is referred to as synchronousreplication. However, not all cells in a culture replicate synchronously. In this case cells do not have multiples of tworeplication forks. Replication initiation is then referred to being asynchronous.[32] However, asynchrony can be caused by mutations to for instanceDnaA[32] orDnaA initiator-associating proteinDiaA.[33]
AlthoughE. coli reproduces bybinary fission the two supposedly identical cells produced by cell division are functionally asymmetric with the old pole cell acting as an aging parent that repeatedly produces rejuvenated offspring.[34] When exposed to an elevated stress level, damage accumulation in an oldE. coli lineage may surpass its immortality threshold so that it arrests division and becomes mortal.[35]Cellular aging is a general process, affectingprokaryotes andeukaryotes alike.[35]
Genetic adaptation
E. coli and related bacteria possess the ability to transferDNA viabacterial conjugation ortransduction, which allows genetic material tospread horizontally through an existing population. The process of transduction, which uses the bacterial virus called abacteriophage,[36] is where the spread of the gene encoding for theShiga toxin from theShigella bacteria toE. coli helped produceE. coli O157:H7, the Shiga toxin-producing strain ofE. coli.
Diversity
E. coli growing on basic cultivation media
E. coli encompasses an enormous population of bacteria that exhibit a very high degree of both genetic and phenotypic diversity.Genome sequencing of many isolates ofE. coli and related bacteria shows that a taxonomic reclassification would be desirable. However, this has not been done, largely due to its medical importance,[37] andE. coli remains one of the most diverse bacterial species: only 20% of the genes in a typicalE. coli genome is shared among all strains.[38]
In fact, from the more constructive point of view, the members of genusShigella (S. dysenteriae,S. flexneri,S. boydii, andS. sonnei) should be classified asE. coli strains, a phenomenon termedtaxa in disguise.[39] Similarly, other strains ofE. coli (e.g. theK-12 strain commonly used inrecombinant DNA work) are sufficiently different that they would merit reclassification.
Astrain is asubgroup within the species that has unique characteristics that distinguish it from otherstrains. These differences are often detectable only at the molecular level; however, they may result in changes to the physiology or lifecycle of the bacterium. For example, a strain may gainpathogenic capacity, the ability to use a uniquecarbon source, the ability to take upon a particularecological niche, or the ability to resistantimicrobial agents. Different strains ofE. coli are often host-specific, making it possible to determine the source of fecal contamination in environmental samples.[13][14] For example, knowing whichE. coli strains are present in a water sample allows researchers to make assumptions about whether the contamination originated from a human, anothermammal, or abird.
A common subdivision system ofE. coli, but not based on evolutionary relatedness, is by serotype, which is based on major surfaceantigens (O antigen: part oflipopolysaccharide layer; H:flagellin; Kantigen: capsule), e.g.O157:H7).[40] It is, however, common to cite only theserogroup, i.e. theO-antigen. At present, about 190 serogroups are known.[41] The common laboratory strain has a mutation that prevents the formation of anO-antigen and is thus not typeable.
Genome plasticity and evolution
Like all lifeforms, new strains ofE. colievolve through the natural biological processes ofmutation,gene duplication, andhorizontal gene transfer; in particular, 18% of the genome of thelaboratory strain MG1655 was horizontally acquired since the divergence fromSalmonella.[42]E. coli K-12 andE. coli B strains are the most frequently used varieties for laboratory purposes. Some strains developtraits that can be harmful to a host animal. Thesevirulent strains typically cause a bout ofdiarrhea that is oftenself-limiting in healthy adults but is frequently lethal to children in the developing world.[43] More virulent strains, such asO157:H7, cause serious illness or death in the elderly, the very young, or theimmunocompromised.[43][44]
The generaEscherichia andSalmonella diverged around 102 million years ago (credibility interval: 57–176 mya), an event unrelated to the much earlier (seeSynapsid) divergence of their hosts: the former being found in mammals and the latter in birds and reptiles.[45] This was followed by a split of anEscherichia ancestor into five species (E. albertii,E. coli,E. fergusonii,E. hermannii, andE. vulneris). The lastE. coli ancestor split between 20 and 30 million years ago.[46]
Thelong-term evolution experiments usingE. coli, begun byRichard Lenski in 1988, have allowed direct observation of genome evolution over more than 65,000 generations in the laboratory.[47] For instance,E. coli typically do not have the ability to grow aerobically withcitrate as acarbon source, which is used as a diagnostic criterion with which to differentiateE. coli from other, closely, related bacteria such asSalmonella. In this experiment, one population ofE. coli unexpectedly evolved the ability to aerobically metabolizecitrate, a major evolutionary shift with some hallmarks of microbialspeciation.
Scanning electron micrograph of anE. coli colony
In the microbial world, a relationship of predation can be established similar to that observed in the animal world. Considered, it has been seen thatE. coli is the prey of multiple generalist predators, such asMyxococcus xanthus. In this predator-prey relationship, a parallel evolution of both species is observed through genomic and phenotypic modifications, in the case ofE. coli the modifications are modified in two aspects involved in their virulence such as mucoid production (excessive production of exoplasmic acid alginate ) and the suppression of theOmpT gene, producing in future generations a better adaptation of one of the species that is counteracted by the evolution of the other, following a co-evolutionary model demonstrated by theRed Queen hypothesis.[48]
Neotype strain
E. coli is the type species of the genus (Escherichia) and in turnEscherichia is the type genus of the familyEnterobacteriaceae, where the family name does not stem from the genusEnterobacter + "i" (sic.) + "aceae", but from "enterobacterium" + "aceae" (enterobacterium being not a genus, but an alternative trivial name to enteric bacterium).[49][50][51]
The original strain described by Escherich is believed to be lost, consequently a new type strain (neotype) was chosen as a representative: the neotype strain is U5/41T,[52] also known under the deposit namesDSM 30083,[53]ATCC 11775,[54] and NCTC 9001,[55] which is pathogenic to chickens and has an O1:K1:H7serotype.[56] However, in most studies, eitherO157:H7, K-12 MG1655, or K-12 W3110 were used as a representativeE. coli. The genome of the type strain has only lately been sequenced.[52]
Phylogeny ofE. coli strains
This section'sfactual accuracy may be compromised due to out-of-date information. The reason given is: Cladogram uses anOR extension of Sims & Kim 2011, which is outdated anyways and should be replaced by Meier-Kolthoff et al. 2014 (fig 6).. Relevant discussion may be found on thetalk page. Please help update this article to reflect recent events or newly available information.(January 2021)
Many strains belonging to this species have been isolated and characterised. In addition to serotype (vide supra), they can be classified according to theirphylogeny, i.e. the inferred evolutionary history, as shown below where the species is divided into six groups as of 2014.[57][58] Particularly the use ofwhole genome sequences yields highly supported phylogenies.[52] Thephylogroup structure remains robust to newer methods and sequences, which sometimes adds newer groups, giving 8 or 14 as of 2023.[59][60]
The link between phylogenetic distance ("relatedness") and pathology is small,[52]e.g. theO157:H7 serotype strains, which form aclade ("an exclusive group")—group E below—are all enterohaemorragic strains (EHEC), but not all EHEC strains are closely related. In fact, four different species ofShigella are nested amongE. coli strains (vide supra), whileE. albertii andE. fergusonii are outside this group. Indeed, allShigella species were placed within a single subspecies ofE. coli in a phylogenomic study that included the type strain.[52] All commonly usedresearch strains ofE. coli belong to group A and are derived mainly from Clifton's K-12 strain (λ+ F+; O16) and to a lesser degree fromd'Herelle's "Bacillus coli" strain (B strain; O7).
There have been multiple proposals to revise the taxonomy to match phylogeny.[52] However, all these proposals need to face the fact thatShigella remains a widely used name in medicine and find ways to reduce any confusion that can stem from renaming.[61]
The first completeDNA sequence of anE. coligenome (laboratory strain K-12 derivative MG1655) was published in 1997. It is a circularDNA molecule 4.6 millionbase pairs in length, containing 4288 annotated protein-coding genes (organized into 2584operons), sevenribosomal RNA (rRNA) operons, and 86transfer RNA (tRNA) genes. Despite having been the subject of intensive genetic analysis for about 40 years, many of these genes were previously unknown. The coding density was found to be very high, with a mean distance between genes of only 118 base pairs. The genome was observed to contain a significant number oftransposable genetic elements, repeat elements, crypticprophages, andbacteriophage remnants.[62] Most genes have only a single copy.[63]
More than three hundred complete genomic sequences ofEscherichia andShigella species are known. The genome sequence of the type strain ofE. coli was added to this collection before 2014.[52] Comparison of these sequences shows a remarkable amount of diversity; only about 20% of each genome represents sequences present in every one of the isolates, while around 80% of each genome can vary among isolates.[38] Each individual genome contains between 4,000 and 5,500 genes, but the total number of different genes among all of the sequencedE. coli strains (the pangenome) exceeds 16,000. This very large variety of component genes has been interpreted to mean that two-thirds of theE. colipangenome originated in other species and arrived through the process of horizontal gene transfer.[64]
Genes inE. coli are usually named in accordance with the uniform nomenclature proposed by Demerec et al.[65] Gene names are 3-letter acronyms that derive from their function (when known) or mutant phenotype and are italicized. When multiple genes have the same acronym, the different genes are designated by a capital later that follows the acronym and is also italicized. For instance,recA is named after its role inhomologous recombination plus the letter A. Functionally related genes are namedrecB,recC,recD etc. The proteins are named by uppercase acronyms, e.g.RecA,RecB, etc. When the genome ofE. coli strain K-12 substr. MG1655 was sequenced, all known or predicted protein-coding genes were numbered (more or less) in their order on the genome and abbreviated by b numbers, such as b2819 (=recD). The "b" names were created after FredBlattner, who led the genome sequence effort.[62] Another numbering system was introduced with the sequence of anotherE. coli K-12 substrain, W3110, which was sequenced in Japan and hence uses numbers starting by JW... (JapaneseW3110), e.g. JW2787 (=recD).[66] Hence,recD = b2819 = JW2787. Note, however, that most databases have their own numbering system, e.g. the EcoGene database[67] uses EG10826 forrecD. Finally, ECK numbers are specifically used for alleles in the MG1655 strain ofE. coli K-12.[67] Complete lists of genes and their synonyms can be obtained from databases such as EcoGene orUniprot.
Proteomics
Proteome
The genome sequence ofE. coli predicts 4288 protein-coding genes, of which 38 percent initially had no attributed function. Comparison with five other sequenced microbes reveals ubiquitous as well as narrowly distributed gene families; many families of similar genes withinE. coli are also evident. The largest family of paralogous proteins contains 80 ABC transporters. The genome as a whole is strikingly organized with respect to the local direction of replication; guanines, oligonucleotides possibly related to replication and recombination, and most genes are so oriented. The genome also contains insertion sequence (IS) elements, phage remnants, and many other patches of unusual composition indicating genome plasticity through horizontal transfer.[62]
Several studies have experimentally investigated theproteome ofE. coli. By 2006, 1,627 (38%) of the predicted proteins (open reading frames, ORFs) had been identified experimentally.[68] Mateus et al. 2020 detected 2,586 proteins with at least 2 peptides (60% of all proteins).[69]
Protein complexes. A 2006 study purified 4,339 proteins from cultures of strain K-12 and found interacting partners for 2,667 proteins, many of which had unknown functions at the time.[71] A 2009 study found 5,993 interactions between proteins of the sameE. coli strain, though these data showed little overlap with those of the 2006 publication.[72]
Binary interactions. Rajagopalaet al. (2014) have carried out systematic yeast two-hybrid screens with mostE. coli proteins, and found a total of 2,234 protein-protein interactions.[73] This study also integrated genetic interactions and protein structures and mapped 458 interactions within 227protein complexes.
Due to the low cost and speed with which it can be grown and modified in laboratory settings,E. coli is a popular expression platform for the production ofrecombinant proteins used in therapeutics. One advantage to usingE. coli over another expression platform is thatE. coli naturally does not export many proteins into theperiplasm, making it easier to recover a protein of interest without cross-contamination.[76] TheE. coli K-12 strains and their derivatives (DH1, DH5α, MG1655, RV308 and W3110) are the strains most widely used by the biotechnology industry.[77] NonpathogenicE. coli strain Nissle 1917 (EcN), (Mutaflor) andE. coli O83:K24:H31 (Colinfant)[78][79]) are used asprobiotic agents in medicine, mainly for the treatment of variousgastrointestinal diseases,[80] includinginflammatory bowel disease.[81] It is thought that the EcN strain might impede the growth of opportunistic pathogens, includingSalmonella and othercoliform enteropathogens, through the production ofmicrocin proteins the production ofsiderophores.[82]
MostE. coli strains do not cause disease, naturally living in the gut,[83] but virulent strains can causegastroenteritis,urinary tract infections,neonatal meningitis, hemorrhagic colitis, andCrohn's disease.[84] Common signs and symptoms include severe abdominal cramps, diarrhea, hemorrhagic colitis, vomiting, and sometimes fever. In rarer cases, virulent strains are also responsible for bowel necrosis (tissue death) and perforation without progressing tohemolytic-uremic syndrome,peritonitis,mastitis,sepsis, and gram-negativepneumonia. Very young children are more susceptible to develop severe illness, such as hemolytic uremic syndrome; however, healthy individuals of all ages are at risk to the severe consequences that may arise as a result of being infected withE. coli.[74][85][86][87]
Some strains ofE. coli, for example O157:H7, can produceShiga toxin. The Shiga toxin causes inflammatory responses in target cells of the gut, leaving behind lesions which result in the bloody diarrhea that is a symptom of aShiga toxin-producingE. coli (STEC) infection. This toxin further causes premature destruction of the red blood cells, which then clog the body's filtering system, the kidneys, in some rare cases (usually in children and the elderly) causinghemolytic-uremic syndrome (HUS), which may lead to kidney failure and even death. Signs of hemolytic uremic syndrome include decreased frequency of urination, lethargy, and paleness of cheeks and inside the lower eyelids. In 25% of HUS patients, complications of nervous system occur, which in turn causesstrokes. In addition, this strain causes the buildup of fluid (since the kidneys do not work), leading toedema around the lungs, legs, and arms. This increase in fluid buildup especially around the lungs impedes the functioning of the heart, causing an increase in blood pressure.[88][86][87]
UropathogenicE. coli (UPEC) is one of the main causes ofurinary tract infections.[89] It is part of the normal microbiota in the gut and can be introduced in many ways. In particular for females, the direction of wiping after defecation (wiping back to front) can lead to fecal contamination of the urogenital orifices. Anal intercourse can also introduce this bacterium into the male urethra, and in switching from anal to vaginal intercourse, the male can also introduce UPEC to the female urogenital system.
EnterotoxigenicE. coli (ETEC) is the most common cause oftraveler's diarrhea, with as many as 840 million cases worldwide in developing countries each year. The bacteria, typically transmitted through contaminated food or drinking water, adheres to theintestinal lining, where it secretes either of two types ofenterotoxins, leading to watery diarrhea. The rate and severity of infections are higher among children under the age of five, including as many as 380,000 deaths annually.[90]
In May 2011, oneE. coli strain,O104:H4, was the subject of abacterial outbreak that began inGermany. Certain strains ofE. coli are a major cause offoodborne illness. The outbreak started when several people in Germany were infected withenterohemorrhagicE. coli (EHEC) bacteria, leading to hemolytic-uremic syndrome (HUS), a medical emergency that requires urgent treatment. The outbreak did not only concern Germany, but also 15 other countries, including regions in North America.[91] On 30 June 2011, the GermanBundesinstitut für Risikobewertung (BfR) (Federal Institute for Risk Assessment, a federal institute within the GermanFederal Ministry of Food, Agriculture and Consumer Protection) announced that seeds offenugreek fromEgypt were likely the cause of the EHEC outbreak.[92]
Some studies have demonstrated an absence of E.coli in the gut flora of subjects with the metabolic disorderPhenylketonuria. It is hypothesized that the absence of these normal bacterium impairs the production of the key vitamins B2 (riboflavin) and K2 (menaquinone) – vitamins which are implicated in many physiological roles in humans such as cellular and bone metabolism – and so contributes to the disorder.[93]
Carbapenem-resistantE. coli(carbapenemase-producingE. coli) that are resistant to thecarbapenem class ofantibiotics, considered thedrugs of last resort for such infections. They are resistant because they produce anenzyme called acarbapenemase that disables the drug molecule.[94]
Incubation period
The time between ingesting the STEC bacteria and feeling sick is called the "incubation period". The incubation period is usually 3–4 days after the exposure, but may be as short as 1 day or as long as 10 days. The symptoms often begin slowly with mild belly pain or non-bloody diarrhea that worsens over several days. HUS, if it occurs, develops an average 7 days after the first symptoms, when the diarrhea is improving.[95]
Diagnosis
Diagnosis of infectious diarrhea and identification of antimicrobial resistance is performed using astool culture with subsequentantibiotic sensitivity testing. It requires a minimum of 2 days and maximum of several weeks to culture gastrointestinal pathogens. The sensitivity (true positive) and specificity (true negative) rates for stool culture vary by pathogen, although a number ofhuman pathogens can not becultured. For culture-positive samples, antimicrobial resistance testing takes an additional 12–24 hours to perform.
Currentpoint of caremolecular diagnostic tests can identifyE. coli and antimicrobial resistance in the identified strains much faster than culture and sensitivity testing. Microarray-based platforms can identify specific pathogenic strains ofE. coli andE. coli-specific AMR genes in two hours or less with high sensitivity and specificity, but the size of the test panel (i.e., total pathogens and antimicrobial resistance genes) is limited. Newermetagenomics-based infectious disease diagnostic platforms are currently being developed to overcome the various limitations of culture and all currently available molecular diagnostic technologies.
Treatment
The mainstay of treatment is the assessment ofdehydration and replacement of fluid and electrolytes. Administration ofantibiotics has been shown to shorten the course of illness and duration of excretion of enterotoxigenicE. coli (ETEC) in adults in endemic areas and in traveller's diarrhea, though the rate of resistance to commonly used antibiotics is increasing and they are generally not recommended.[96] The antibiotic used depends upon susceptibility patterns in the particular geographical region. Currently, the antibiotics of choice arefluoroquinolones orazithromycin, with an emerging role forrifaximin. Rifaximin, a semisynthetic rifamycin derivative, is an effective and well-tolerated antibacterial for the management of adults with non-invasive traveller's diarrhea. Rifaximin was significantly more effective than placebo and no less effective thanciprofloxacin in reducing the duration of diarrhea. While rifaximin is effective in patients withE. coli-predominant traveller's diarrhea, it appears ineffective in patients infected with inflammatory or invasiveenteropathogens.[97]
Prevention
ETEC is the type ofE. coli that most vaccine development efforts are focused on.Antibodies against the LT and major CFs of ETEC provide protection against LT-producing, ETEC-expressinghomologous CFs. Oral inactivated vaccines consisting of toxin antigen and whole cells, i.e. the licensed recombinant cholera B subunit (rCTB)-WC cholera vaccine Dukoral, have been developed. There are currently no licensed vaccines for ETEC, though several are in various stages of development.[98] In different trials, the rCTB-WC cholera vaccine provided high (85–100%) short-term protection. An oral ETEC vaccine candidate consisting of rCTB and formalin inactivatedE. coli bacteria expressing major CFs has been shown in clinical trials to be safe, immunogenic, and effective against severediarrhoea in American travelers but not against ETEC diarrhoea in young children inEgypt. A modified ETEC vaccine consisting of recombinantE. coli strains over-expressing the major CFs and a more LT-like hybrid toxoid called LCTBA, are undergoing clinical testing.[99][100]
Other proven prevention methods forE. coli transmission include handwashing and improved sanitation and drinking water, as transmission occurs through fecal contamination of food and water supplies. Additionally, thoroughly cooking meat and avoiding consumption of raw, unpasteurized beverages, such as juices and milk are other proven methods for preventingE. coli. Lastly, cross-contamination of utensils and work spaces should be avoided when preparing food.[101]
Escherichia coli bacterium, 2021, Illustration by David S. Goodsell, RCSB Protein Data Bank This painting shows a cross-section through anEscherichia coli cell. The characteristic two-membrane cell wall of gram-negative bacteria is shown in green, with many lipopolysaccharide chains extending from the surface and a network of cross-linked peptidoglycan strands between the membranes. The genome of the cell forms a loosely-defined "nucleoid", shown here in yellow, and interacts with many DNA-binding proteins, shown in tan and orange. Large soluble molecules, such as ribosomes (colored in reddish purple), mostly occupy the space around the nucleoid.
E. coli is a very versatile host for the production ofheterologousproteins,[104] and variousprotein expression systems have been developed which allow the production ofrecombinant proteins inE. coli. Researchers can introduce genes into the microbes using plasmids which permit high level expression of protein, and such protein may be mass-produced inindustrial fermentation processes. One of the first useful applications of recombinant DNA technology was the manipulation ofE. coli to produce humaninsulin.[105]
Many proteins previously thought difficult or impossible to be expressed inE. coli in folded form have been successfully expressed inE. coli. For example, proteins with multiple disulphide bonds may be produced in theperiplasmic space or in the cytoplasm of mutants rendered sufficiently oxidizing to allow disulphide-bonds to form,[106] while proteins requiringpost-translational modification such asglycosylation for stability or function have been expressed using the N-linked glycosylation system ofCampylobacter jejuni engineered intoE. coli.[107][108][109]
Strain K-12 is a mutant form ofE. coli that over-expresses the enzymeAlkaline phosphatase (ALP).[112] The mutation arises due to a defect in the gene that constantly codes for the enzyme. A gene that is producing a product without any inhibition is said to haveconstitutive activity. This particular mutant form is used to isolate and purify the aforementioned enzyme.[112]
Strain OP50 ofEscherichia coli is used for maintenance ofCaenorhabditis elegans cultures.
Strain JM109 is a mutant form ofE. coli that is recA and endA deficient. The strain can be utilized for blue/white screening when the cells carry the fertility factor episome.[113] Lack of recA decreases the possibility of unwanted restriction of the DNA of interest and lack of endA inhibit plasmid DNA decomposition. Thus, JM109 is useful for cloning and expression systems.
Model organism
Helium ion microscopy image showingT4 phage infectingE. coli. Some of the attached phage have contracted tails indicating that they have injected their DNA into the host. The bacterial cells are ~ 0.5 μm wide.[114]
E. coli is frequently used as a model organism inmicrobiology studies. Cultivated strains (e.g.E. coli K12) are well-adapted to the laboratory environment, and, unlikewild-type strains, have lost their ability to thrive in the intestine. Many laboratory strains lose their ability to formbiofilms.[115][116] These features protect wild-type strains fromantibodies and other chemical attacks, but require a large expenditure of energy and material resources.E. coli is often used as a representative microorganism in the research of novel water treatment and sterilisation methods, includingphotocatalysis. By standardplate count methods, following sequential dilutions, and growth on agar gel plates, the concentration of viable organisms or CFUs (Colony Forming Units), in a known volume of treated water can be evaluated, allowing the comparative assessment of materials performance.[117]
In 1946,Joshua Lederberg andEdward Tatum first described the phenomenon known asbacterial conjugation usingE. coli as a model bacterium,[118] and it remains the primary model to study conjugation.[119]E. coli was an integral part of the first experiments to understandphage genetics,[120] and early researchers, such asSeymour Benzer, usedE. coli and phage T4 to understand the topography of gene structure.[121] Prior to Benzer's research, it was not known whether the gene was a linear structure, or if it had a branching pattern.[122]
E. coli was one of the first organisms to have its genome sequenced; the complete genome ofE. coli K12 was published byScience in 1997.[62]
MDS42
From 2002 to 2010, a team at the Hungarian Academy of Science created a strain ofEscherichia coli called MDS42, which is now sold by Scarab Genomics of Madison, WI under the name of "Clean GenomeE. coli",[123] where 15% of the genome of the parental strain (E. coli K-12 MG1655) were removed to aid in molecular biology efficiency, removingIS elements,pseudogenes andphages, resulting in better maintenance of plasmid-encoded toxic genes, which are often inactivated by transposons.[124][125][126] Biochemistry and replication machinery were not altered.
By evaluating the possible combination ofnanotechnologies withlandscape ecology, complex habitat landscapes can be generated with details at the nanoscale.[127] On suchsynthetic ecosystems, evolutionary experiments withE. coli have been performed to study the spatial biophysics of adaptation in anisland biogeography on-chip.
In other studies, non-pathogenicE. coli has been used as a model microorganism towards understanding the effects of simulated microgravity (on Earth) on the same.[128][129]
Uses in biological computing
Since 1961, scientists proposed the idea of genetic circuits used for computational tasks. Collaboration between biologists and computing scientists has allowed designing digital logic gates on the metabolism ofE. coli. AsLac operon is a two-stage process, genetic regulation in the bacteria is used to realize computing functions. The process is controlled at the transcription stage of DNA into messenger RNA.[130]
Studies are being performed attempting to programE. coli to solve complicated mathematics problems, such as theHamiltonian path problem.[131]
A computer to control protein production ofE. coli withinyeast cells has been developed.[132] A method has also been developed to use bacteria to behave as anLCD screen.[133][134]
In July 2017, separate experiments withE. coli published on Nature showed the potential of using living cells for computing tasks and storing information.[135] A team formed with collaborators of theBiodesign Institute atArizona State University and Harvard'sWyss Institute for Biologically Inspired Engineering developed a biological computer insideE. coli that responded to a dozen inputs. The team called the computer "ribocomputer", as it was composed ofribonucleic acid.[136][137] Meanwhile, Harvard researchers probed that is possible to store information in bacteria after successfully archiving images and movies in the DNA of livingE. coli cells.[138][139] In 2021, a team led by biophysicist Sangram Bagh realized a study withE. coli to solve2 × 2 maze problems to probe the principle fordistributed computing among cells.[140][141]
History
In 1885, the German-Austrian pediatricianTheodor Escherich discovered this organism in the feces of healthy individuals. He called itBacterium coli commune because it is found in the colon. Early classifications ofprokaryotes placed these in a handful of genera based on their shape and motility (at that timeErnst Haeckel's classification of bacteria in the kingdomMonera was in place).[100][142][143]
Bacterium coli was the type species of the now invalid genusBacterium when it was revealed that the former type species ("Bacterium triloculare") was missing.[144] Following a revision ofBacterium, it was reclassified asBacillus coli by Migula in 1895[145] and later reclassified in the newly created genusEscherichia,named after its original discoverer, byAldo Castellani andAlbert John Chalmers.[146]
In 2024, an outbreak ofE. coli food poisoning occurred across the U.S. was linked toU.S.-grown organiccarrots causing one fatality and dozens of illnesses.[149]
Uses
E. coli has several practical uses besides its use as a vector for genetic experiments and processes. For example,E. coli can be used to generate synthetic propane and recombinant human growth hormone.[150][151]
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