What Are Biological Mutant Agents?

What Are Biological Mutant Agents?

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Biological agents of mutations

Transposon is a section of DNA that undergoes
autonomous fragment relocation/multiplication.
Its insertion into chromosomal DNA disrupts
functional elements of the genes.

Virus– Virus DNA may be inserted into the
genome which disrupts genetic function.

Infectious agents have been suggested to cause
cancer as early as 1908 by Vilhelm Ellermann
and Oluf Bang, and 1911 by Peyton Rous who
discovered the Rous sarcoma virus.

Bacteria– some bacteria such as Helicobacter
pylori cause inflammation during which oxidative
species are produced, causing DNA damage and
reducing efficiency of DNA repair systems,
thereby increasing mutation.
7 months ago
Biological mutant agents are substances
that change the genetic material of
organisms, such as DNA, and include certain
chemicals and rays, such as ultraviolet
radiation, X-rays and gamma rays, along
with viruses and bacteria. Many mutagenic
agents cause cancer, and are dually
classified as carcinogens. While mutant
agents cause artificial changes in genetic
codes and replication, some mutations
occur naturally and are caused by
spontaneous hydrolysis and errors in DNA
replication, recombination and repair.
Malicious viruses and bacteria are the most
common types of biological agents. Viruses
act as agents by improperly reading DNA,
and inserting erroneous codes into the
affected genome. This, in turn, alters the
correct functioning of genetic reproduction
and may cause short-term or long-term
health consequences. Some viruses are
more virulent than others, and some cause
more severe symptoms. Viruses produce
different symptoms, such as flu-like
conditions, fevers, and gastrointestinal
issues. In addition to viruses, bacteria also
act as biological agents. Bacteria, like
viruses, vary in duration and the type and
degree of harm they cause to affected
organisms. Bacteria generally damage
vulnerable DNA strands, which in turn
reduces the efficiency of DNA repair systems.
Reduced or impaired repairs, in turn,
increases the risk of mutation. Some
minerals, vitamins and antibiotics provide
some protection against the development
and spread of mutagens within and
between organisms
mhz vee
7 months ago
The development and function of an organism is in large part controlled by genes. Mutations can lead to changes in the structure of an encoded protein or to a decrease or complete loss in its expression. Because a change in the DNA sequence affects all copies of the encoded protein, mutations can be particularly damaging to a cell or organism. In contrast, any alterations in the sequences of RNA or protein molecules that occur during their synthesis are less serious because many copies of each RNA and protein are synthesized.

Geneticists often distinguish between the genotype and phenotype of an organism. Strictly speaking, the entire set of genes carried by an individual is its genotype, whereas the function and physical appearance of an individual is referred to as its phenotype. However, the two terms commonly are used in a more restricted sense: genotype usually denotes whether an individual carries mutations in a single gene (or a small number of genes), and phenotype denotes the physical and functional consequences of that genotype.

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Mutations Are Recessive or Dominant
A fundamental genetic difference between organisms is whether their cells carry a single set of chromosomes or two copies of each chromosome. The former are referred to as haploid; the latter, as diploid. Many simple unicellular organisms are haploid, whereas complex multicellular organisms (e.g., fruit flies, mice, humans) are diploid.

Different forms of a gene (e.g., normal and mutant) are referred to as alleles. Since diploid organisms carry two copies of each gene, they may carry identical alleles, that is, be homozygous for a gene, or carry different alleles, that is, be heterozygous for a gene. A recessive mutation is one in which both alleles must be mutant in order for the mutant phenotype to be observed; that is, the individual must be homozygous for the mutant allele to show the mutant phenotype. In contrast, the phenotypic consequences of a dominant mutation are observed in a heterozygous individual carrying one mutant and one normal allele
7 months ago
Genomes of bacteria exist on a single double-stranded circular DNA molecule that contains approximately 4000 kb of DNA and are regulated by operons. A mutation is a change in the nucleotide sequence and can create new cellular functionalities or lead to the dysfunction of others. Mutations can occur spontaneously or be caused by exposure to mutation-inducing agents. [1]

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While the majority of bacterial genes exist on one circular chromosome, there are other genetic elements within the bacterial genome. Elements like plasmids, transposons, integrons, or gene cassettes are shorter sequences that mainly contribute to recombination events. Bacterial DNA replication and transcription co-occur and utilize the same template DNA. Replication forks proceed bi-directionally with a single origin of replication, OriC.

Bacterial genes with similar functions often share one promoter (RNA polymerase binding site) and are transcribed simultaneously; this system is called an operon. Typical operons consist of several structural genes that code for the enzymes required for the pathway. Regulation occurs through transcription factors binding to a short sequence of DNA between the promoter region and the structural genes called an operator [2].

A mutation is a change in the nucleotide sequence of a short region of a genome, and phenotypic results may vary on the severity and location of the mutation. Mutations can be the result of errors during DNA replication or induced by exposure to mutagens (like chemicals and radiation). Spontaneous mutations occur at a rate of 1 in 10^5 to 10^8 and contribute to random population variation [3]. Since bacteria are haploid for the majority of their genes and have short generation turnover, phenotypic variation due to point mutations can occur relatively quickly.

Results of mutations can produce changes in structural or colony characteristics or loss in sensitivity to antibiotics. Some potential consequences of mutations are as follows:

Auxotrophs: have a mutation which leaves an essential nutrient process dysfunctional.
Resistant mutants: can withstand the stress of exposure to inhibitory molecules or antibiotics secondary to acquired mutation.
Regulatory mutants: have disruptions on regulatory sequences like promotor regions.
Constitutive mutants: continuously express genes that usually switch on and off as in operons.
Spontaneous Mutations

Spontaneous mutations occur without mutation induction and are the result of errors during DNA replication. When DNA Pol III is synthesizing a new strand of DNA, occasionally a nucleotide will be mispaired, added, or omitted [4]. Thus a point mutation will occur. For example, when nucleotides are mispaired, it will appear that one nucleotide substitutes for another leading to one mutated granddaughter DNA strand. Two separate malfunctions must happen in the bacteria's DNA replication machinery for this to occur [5]:

DNA pol III pairs an incorrect complementary nucleotide base onto the parent strand in the replication fork
The chemical activity of the mispairing is not enough to slow the polymerase portion of DNA polymerase so that the exonuclease can remove the mispair
Studies with Escherichia coli show that spontaneous mutations occur 20 times more often on the lagging strand than leading strand [6].
DNA bases can exist in many different forms, referred to as tautomers. Nucleotide bases dominantly exist in the keto (C-O) and amino (C-NH2) forms, while the imino (C≡NH) and enol (C-OH) occur rarely. Tautomerization, during DNA replication, will alter nucleotide base pair formation. For example, assume that thymine undergoes keto-enol tautomerization during replication. This enol species will preferentially bind to guanine during the first replication cycle. Due to the semiconservative nature of DNA replication, at the end of the 2nd round of replication, there will be (3) A-T base pairs and (1) G-C in the locus of mutation [7].

The mechanism is as follows:

T – A --> Tautomerization --> T' – A --> replication 1 --> T' – G and A –T

T – G --> Replication 2 --> T – A and G – C

(enol form of thymine indicated as T') [8]

Errors in DNA replication can result in the addition of erroneous nucleotides or deletion of template nucleotides. For example, loci with a high number of short repeat nucleotides are prone to polymerase slippage. During replication, the DNA Pol III temporarily dissociates from the template strand. Along with its newly synthesized strand, the DNA Polymerase may relocate a few repeats upstream or downstream of its original locus. Slip strand mispairing can result in addition/deletion mutations because some nucleotides are replicated twice while others do not replicate. If the repeats are not in a multiple of three, the mutation can result in a frameshift (A shift in the coding sequence downstream of the mutation). These mutations lead to loss of normal protein functionality. Slip-strand mispairings can increase variation of short tandem repeats (STRs) in a bacterial population and are useful in genetic testing. When an addition or deletion occurs, the potential genomic outcomes are as follows [9]:

Silent mutation: The mutation changes the original codon into another codon that codes for the same amino acid
Missense mutation: When a mutation in the sequence causes a codon to code for a different amino acid
Nonsense mutation: A mutant stop codon replaces a wild-type codon, which terminates translation resulting in a shortened protein.
The mutation's phenotypical severity depends on the structure of the substituted amino acid's effect on the final protein product. More specifically, non-synonymous amino acid substitutions produce dramatic changes in protein structures because of the chemical dis-similarities of the mutated strand amino acid. However, there are inherent protections against these types of mutations. The redundancy of codon translation mechanisms and occurrence of non-coding regions result in few mutations expressing phenotypically [10].

Mutation Induction

Mutagens may be of physical, chemical, or of biological origin. Mostly they act on the DNA directly, causing damage which may result in errors during replication. Although, severely damaged DNA can prevent replication and cause cell death. SOS is an example of a cellular response to DNA damage that results in cell cycle arrest and induction of mutagenesis. Rec A induces SOS response by recognizing single-stranded DNA and activating mutagenic DNA polymerases (II, IV, and V) [11].

The following are several classes of mutagens and their subsequent effects :

Physical Mutagens

Examples of physical mutagens include radiation or UV exposure. UV radiation damages DNA by creating covalent linkages between adjacent pyrimidine bases. This pyrimidine dimer cannot fit well in the double helix structure of DNA and thus inhibiting replication and translation. However, dimer formation usually results in a deletion mutation. Other types of radiation can have a variety of effects (Depending on intensity and wavelength), but mostly insertions/deletions occur. Purine dimers rarely occur [12].

Chemical Mutagens

Chemical mutagens are agents that either directly or indirectly induce mutations [13]. A chemical mutagen can either replace a base in DNA, alter a base's composition and pairing behavior, or damage the base so that it can no longer pair. These include DNA reactive chemicals such as those listed below:

Base analogs:

Structurally similar enough to nucleotides in that they can incorporate into DNA. For example, 5-bromouracil, an analog of thymine, acts as a substrate during DNA replication and causes point mutations. This mispairing occurs because the base analog forms a tautomer and pairs with guanine instead of adenine [14].

Reactive oxygen species:

Hydroxyl radicals attack guanine thereby producing 8-hydroxy-deoxyguanosine (8-OhdG) which mispairs with adenine instead of cytosine which resulting in a (G -> T) transversion during replication [15].

Deaminating agents:

These agents remove amino groups on nucleotide bases. Deaminating agents produce an adenine species that pairs with cytosine and a cytosine species (Uracil) that pairs to adenine. Deamination of guanine results in xanthine which inhibits replication, thereby not creating a mutation [15].

Flat aromatic compounds:

Acridines like ethidium bromide can intercalate with adjacent pyrimidine base pairs. This interaction slightly unwinds the helix and increases the distance between adjacent base pairs. This intercalation disrupts the reading frame during translation and can cause insertions or deletions [16].

Alkylating agents:

Agents like ethyl methanesulfonate and dimethyl nitrosoguanidine alter the nucleotide base by adding alkyl groups. The nature and position of the alkylation can vary but usually leads to point mutations through base mispairing. However, alkylation can cause crosslink formation which inhibits replication.

Biological Mutagens

Biological agents of mutation are sources of DNA from elements like transposons and viruses. Transposons are sequences of DNA that can relocate and replicate autonomously. Insertion of a transposon into a DNA sequence can disrupt gene functionality. Transposition is not technically a type of recombination but is mechanistically similar. Transposons often pair with short regions of nucleotide repeats on either side of the transposition sequence [1]. There are three types of transposons:

Replicative transposons keep the original locus and translocate a copy
Conservative transposons occur when the original transposon translocates
Retrotransposons transpose via RNA inter
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