A plasmid is a small DNA molecule that is physically separate from, and can replicate independently of, chromosomal DNA within a cell. In microbiology and genetics, a plasmid is a DNA molecule that is separate from, and can replicate independently of the chromosomal DNA. They are double-stranded and, in many cases, circular. Plasmids usually occur naturally in bacteria, but are sometimes found in archaea, and even in eukaryotic organisms e. Step by step of cloning a gene using a plasmid : This image shows a line drawing that compares the activity of non-integrating plasmids, on the top, with episomes, on the bottom, during cell division.
The upper half of the image shows a bacterium with its chromosomal DNA and plasmids dividing into two identical bacteria, each with their chromosomal DNA and plasmids. The lower half of the image shows a bacterium with its chromosomal DNA, but with an episome. Next to this bacterium, we see the same bacterium, but after the episome has integrated into the chromosomal DNA and has become a part of it.
This second bacterium now divides into two bacteria identical to it, each with an episome integrated into it. Plasmid sizes vary from 1 to over 1, kbp. The number of identical plasmids in a single cell can range anywhere from one to thousands under some circumstances. Plasmids can be considered part of the mobilome because they are often associated with conjugation, a mechanism of horizontal gene transfer. The term plasmid was first introduced by the American molecular biologist Joshua Lederberg in Plasmids are considered replicons.
They can be found in all three major domains: Archaea, Bacteria, and Eukarya. Similar to viruses, plasmids are not considered by some to be a form of life. There is insufficient documentation shedding light on transformation, which occurs in natural microbial habitats.
Greaves and Wilson have, however, demonstrated that nucleic acids become adsorbed to soil clay minerals, particularly to montmorillonite, and that the adsorption protects the nucleic acids from degradation by enzymes. Similarly clay adsorbed viruses, proteins, peptides, and amino acids are protected to different degrees against microbial degradation.
Accordingly, both naked DNA taking part in transduction may endure in natural habitats despite the absence of an appropriate host [ 23 ]. This adsorption to clay minerals protecting soluble organics and viruses from degradation is vital to consider in any possible exchange of genes occurring in clay containing habitats and other surface-active particulates.
An inability of transforming DNA and transducing viruses to survive can be expected for long in natural habitats lacking hosts. In addition, being best, the substrate for nonhost microbes that is they contain C, N, and P as well as S in case of viruses means they would be swiftly degraded by the indigenous microbiota. However, there is growing evidence that DNA and viruses persevere in natural habitats due to the clay minerals adsorption process, which protects against both biological inactivation and physico-chemical.
Thus, if transforming DNA and viruses no studies have investigated the ability of adsorbed DNA to transform are able to persist in natural habitats, it is possible that it is through transmission of their genetic information to any suitable host introduced into these habitats inadvertently or deliberately. There are sporadic studies involving the survival and consequent microbial establishment of microbes, which do not inhabit a particular habitat.
This is illustrated by the survival ability of enteric bacteria including E. It cannot be said that plasmids are mere materials and a suitable environment for genetic exchange given that they themselves are subjects to evolutionary forces [ 24 ]. The connections of plasmid access in new bacteria result in a cost of fitness. Therefore, if the plasmid is unable to spread horizontally with the required speed ensuring its survival as a pure gene parasite, the theory predicts that it will be removed from the bacterial group.
Thus, unless the plasmid-encoded traits are not selected, the plasmid of the population will be removed by purifying the selection.
Furthermore, positive selections can ultimately result in any beneficial plasma genes to move to the bacterial chromosome; hence, the beneficial value of the plasmid is elminiated. However, the costs inflicted by plasmids are not irreversible. In fact, the latest reports indicate that compensatory development can often improve these costs.
Extensive studies conducted by clinical microbiologists have shed light on the molecular basis and epidemiology of AR, giving a clear perception of which genes and AR plasmids proliferate in clinical conditions. In this process, the plasmid bacteria acquire genetic charge that can provide feature. Plasmids typically impose the cost of fitness in the absence encoded properties, and compensatory mutations can constrain the spread of cloning of bacterial plasmids.
This cost can be moderated over time. It is suggested that the significant relation detected between AR plasmids and clinically significant bacteria should be determined with the use of plasmid compensatory development and fitness costs.
Therefore, hospital patients are provided, through dark microbes, with an exclusive opportunity to study a bacterial community described as clinically relevant [ 25 ]. Plasmids are known to be extra chromosomal genetic elements where their ecology and evolution are dependent on their host interaction as well as their genetic repertoire. Mobility and stability are qualities, which influence the plasmid lifestyle and each differs in magnitude.
The relationship between plasmid traits and host biology are caused for transitions between the lifestyles, host range, invasion, persistence, and adaptation of the plasmids. In terms of plasmid ecology, kinetics is an important factor, and as for long-term plasmid evolution, plasmid stability is more relevant. Upon the transition into additional chromosomes, plasmids become no longer independent entering the host lineage. Plasmid evolution of prokaryotic chromosomes may be independent even though they are confined to their hosts.
Evolution of plasmid genome within the host cell occurs after plasmids have successfully entered a host. The plasmid lifestyle is eventually affected by these molecular changes, with outcomes being seen in the development of host range, plasmid adaptation and persistence, and the transition into additional chromosomes [ 26 , 27 , 28 ].
Confluence and clustering of various survival and propagation functions, arranged in functional modules, affect plasmid organization. The initial step to better understand the developmental elements of clinically significant plasmid bacterium affiliations is to acquire an exact gauge of the appropriation of wellness impacts of AR plasmids in their regular bacterial hosts. There are different possible ways to deal with this dissemination in accumulations of intestinal microbiota segregates.
A highly evident methodology is to contemplate the wellness impacts of the plasmids officially found in the clones. This methodology needs the capacity to evacuate fix the plasmid followed by contrasting the overall wellness of clones and without it.
Relieving plasmids from wild-type clinical strains is testing, yet there are new innovations accessible. The issue presenting itself in expelling the plasmid is given that it is difficult to determine to what extent a plasmid has been available in a bacterial clone, and it is additionally difficult to know whether any expense initially forced by the plasmid has just been reduced by compensatory development.
An option is to build a new relationship by joining predominant bacterial clones with AR plasmids from the intestinal microbiome, empowering investigation of the wellness impacts of plasmids upon entry in their hosts.
The enhancement of plasmid costs after some time by means of compensatory changes in the plasmid or bacterial chromosome is inevitable in test show frameworks. It is hence sensible to expect that if plasmids create an expense for their new has in the intestinal microbiome, this expense will be managed by compensatory advancement.
It ought to be conceivable to affirm this speculation by concentrate fleeting arrangement of intestinal microbiota segregates from hospitalized patients.
A lessening after some time in the expense at first forced by a plasmid found in a clone could show an occasion of interpatient compensatory development.
Critically, testing various provinces of the plasmid-conveying clone per time point should build the odds of recuperating remunerated clones. Uncovering potential compensatory transformations aggregated after some time can come from sequencing the bacterial genomes from this worldly arrangement of separates.
At long last, remaking of these changes in the genealogical plasmid-conveying clone will affirm their job [ 27 ]. In nature, gene dissemination by the means of horizontal gene transfer encompasses several different factors plasmids, transposons, integrons, and phages and mechanisms homologous and site-specific recombination, conjugation, transposition, transduction, and transformation [ 26 , 27 , 28 ].
In terms of their genetic organization, plasmids seem to equally possess characteristics of both phages and chromosomes. More studies should concentrate on the regulation networks of conjugative plasmids with the purpose of confirming the existence of a global organization present in their genomes, as an alternative to a meager combination of independent modules [ 29 ]. The ability of a plasmid to facilitate retrotransfer acquire potentially beneficial genes to its host is to a greater extent common in numerous conjugative plasmids.
IncP plasmids are mainly used to study retrotransfer, but it is more noticeable for some newly defined BHR plasmids. Respond to or comment on this page on our feeds on Facebook , Instagram or Twitter. Facebook Twitter Donate to WiB. Plasmid Definition A plasmid is a small double-stranded unit of DNA, usually circular but sometimes linear, that exists independent of the chromosome and is capable of self-replication.
Date Event People Places Datta was a microbial geneticist who showed that multi-antibiotic resistance was transferred between bacteria by plasmids. She first made the connection in after investigating a severe outbreak of Salmonella typhimurium phage-type 27 at Hammersmith Hospital where she worked.
This involved an examination of cultures, of which she found 25 were drug resistant, eight of which were resistant to Streptomycin which had been used to treat the patients.
She concluded that the antibiotic resistance developed over time because the earlier cultures of the salmonella typhimurium infection from the start of the outbreak were not drug resistant. This was based on some experiments he performed with Edward Tatum in which involved mixing two different strains of bacteria.
Their experiments also demonstrated for the first time that bacteria reproduced sexually, rather than by cells splitting in two, thereby proving that bacterial genetic systems were similar to those of multicelluar organisms.
Later on, in , working with Norton Zinder, Lederberg found that certain bacteriophages viruses that affect bacteria could carry a bacterial gene from one bacterium to another.
In Lederberg shared the Nobel Prize for Medicine for 'discoveries concerning genetic recombination and the organisation of the genetic material of bacteria.
During the s he demonstrated that bacteria could acquire resistance by swapping genetic material via plasmids, small microbial DNA molecules. He studied a wide variety bacteria, from diarrhoea-causing E.
Research conducted by Naomi Datta and E S Anderson showed that the R transfer factor plasmid contributed to the rise in resistance. Watanabe Keito University Drug resistant bacteria were first identified in Japan and then in Britain. Some of the earliest observations of this phenomenon were made by Naomi Datta who in showed that structures with some similarity to phages could transfer drug-resistance genes.
Ephraim Anderson, director of the Enteric Reference Laboratory in Colindale, London, subsequently showed that genetic factors endowing resistance to major drugs used against human disease could be transferred by plasmids from minor pathogens. A summary of the work was published in ES Anderson, 'Origin of transferable drug-resistance in the enterobacteriaceae', British Medical Journal, 27 Nov , Plasmids may be passed between different bacterial cells. Small pieces of DNA, such as human DNA, can be attached to appropriate elements, circularized, and then introduced into bacteria, where they are propagated--or in other words, copied--along with the host bacterial chromosome.
These small circles containing the cloned DNA are called plasmids.
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