Identify Two General Ways Chemical Mutagens Can Alter Dna.

9.5: Mutations

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skills to develop

Compare betoken mutations and frameshift mutations
Describe the differences between missense, nonsense, and silent mutations
Describe the differences between low-cal and dark repair
Explain how different mutagens act
Explicate why the Ames exam can exist used to detect carcinogens
Analyze sequences of DNA and identify examples of types of mutations
e following laws within the Ideal Gas Law

A mutation is a heritable alter in the Deoxyribonucleic acid sequence of an organism. The resulting organism, called a mutant, may take a recognizable change in phenotype compared to the wild blazon, which is the phenotype nearly commonly observed in nature. A change in the DNA sequence is conferred to mRNA through transcription, and may lead to an contradistinct amino acid sequence in a protein on translation. Because proteins carry out the vast bulk of cellular functions, a change in amino acid sequence in a protein may lead to an altered phenotype for the jail cell and organism.

Effects of Mutations on DNA Sequence

There are several types of mutations that are classified co-ordinate to how the Deoxyribonucleic acid molecule is altered. I blazon, called a indicate mutation, affects a unmarried base and near unremarkably occurs when one base is substituted or replaced by another. Mutations besides result from the addition of one or more bases, known as an insertion, or the removal of one or more bases, known as a deletion.

Exercise \(\PageIndex{1}\)

What blazon of a mutation occurs when a gene has ii fewer nucleotides in its sequence?

Furnishings of Mutations on Protein Construction and Function

Point mutations may have a wide range of effects on protein part (Effigy \(\PageIndex{one}\)). Equally a issue of the degeneracy of the genetic code, a signal mutation will commonly result in the same amino acid being incorporated into the resulting polypeptide despite the sequence change. This modify would have no effect on the protein's construction, and is thus called a silent mutation. A missense mutation results in a different amino acid existence incorporated into the resulting polypeptide. The effect of a missense mutation depends on how chemically different the new amino acid is from the wild-type amino acid. The location of the changed amino acid within the poly peptide besides is important. For instance, if the changed amino acid is part of the enzyme's active site, then the upshot of the missense mutation may exist significant. Many missense mutations result in proteins that are still functional, at least to some degree. Sometimes the effects of missense mutations may be only credible nether certain environmental conditions; such missense mutations are called conditional mutations. Rarely, a missense mutation may be beneficial. Under the right environmental conditions, this type of mutation may give the organism that harbors it a selective reward. Yet another type of point mutation, called a nonsense mutation, converts a codon encoding an amino acrid (a sense codon) into a cease codon (a nonsense codon). Nonsense mutations result in the synthesis of proteins that are shorter than the wild type and typically non functional.

Deletions and insertions also crusade various effects. Because codons are triplets of nucleotides, insertions or deletions in groups of three nucleotides may lead to the insertion or deletion of ane or more amino acids and may not cause significant furnishings on the resulting protein's functionality. Withal, frameshift mutations, caused by insertions or deletions of a number of nucleotides that are not a multiple of three are extremely problematic because a shift in the reading frame results (Figure \(\PageIndex{1}\)). Because ribosomes read the mRNA in triplet codons, frameshift mutations can alter every amino acid afterwards the signal of the mutation. The new reading frame may also include a terminate codon before the finish of the coding sequence. Consequently, proteins fabricated from genes containing frameshift mutations are nearly always nonfunctional.

Effigy \(\PageIndex{1}\): Mutations can lead to changes in the protein sequence encoded by the DNA.

Exercise \(\PageIndex{2}\)

What are the reasons a nucleotide modify in a cistron for a protein might not have any effect on the phenotype of that gene?
Is information technology possible for an insertion of three nucleotides together after the fifth nucleotide in a protein-coding factor to produce a protein that is shorter than normal? How or how not?

A Beneficial MUTATION

Since the beginning example of infection with human immunodeficiency virus (HIV) was reported in 1981, nearly twoscore 1000000 people accept died from HIV infection,¹ the virus that causes caused immune deficiency syndrome (AIDS). The virus targets helper T cells that play a primal role in bridging the innate and adaptive immune response, infecting and killing cells normally involved in the torso's response to infection. At that place is no cure for HIV infection, but many drugs accept been developed to boring or block the progression of the virus. Although individuals around the world may be infected, the highest prevalence among people 15–49 years old is in sub-Saharan Africa, where nearly one person in 20 is infected, accounting for greater than 70% of the infections worldwide^two (Figure \(\PageIndex{ii}\)). Unfortunately, this is too a part of the world where prevention strategies and drugs to treat the infection are the most lacking.

Figure \(\PageIndex{ii}\): HIV is highly prevalent in sub-Saharan Africa, just its prevalence is quite depression in some other parts of the world.

In recent years, scientific interest has been piqued past the discovery of a few individuals from northern Europe who are resistant to HIV infection. In 1998, American geneticist Stephen J. O'Brien at the National Institutes of Health (NIH) and colleagues published the results of their genetic analysis of more than 4,000 individuals. These indicated that many individuals of Eurasian descent (up to 14% in some ethnic groups) take a deletion mutation, chosen CCR5-delta 32, in the factor encoding CCR5. CCR5 is a coreceptor found on the surface of T cells that is necessary for many strains of the virus to enter the host cell. The mutation leads to the product of a receptor to which HIV cannot effectively bind and thus blocks viral entry. People homozygous for this mutation have greatly reduced susceptibility to HIV infection, and those who are heterozygous have some protection from infection also.

It is not clear why people of northern European descent, specifically, carry this mutation, just its prevalence seems to be highest in northern Europe and steadily decreases in populations every bit one moves south. Research indicates that the mutation has been present since before HIV appeared and may accept been selected for in European populations equally a consequence of exposure to the plague or smallpox. This mutation may protect individuals from plague (caused by the bacterium Yersinia pestis) and smallpox (caused by the variola virus) because this receptor may also exist involved in these diseases. The age of this mutation is a matter of contend, but estimates propose it appeared between 1875 years to 225 years ago, and may have been spread from Northern Europe through Viking invasions.

This exciting finding has led to new avenues in HIV research, including looking for drugs to block CCR5 binding to HIV in individuals who lack the mutation. Although Dna testing to determine which individuals acquit the CCR5-delta 32 mutation is possible, there are documented cases of individuals homozygous for the mutation contracting HIV. For this reason, Deoxyribonucleic acid testing for the mutation is not widely recommended past public health officials and so every bit not to encourage risky behavior in those who conduct the mutation. Nonetheless, inhibiting the bounden of HIV to CCR5 continues to be a valid strategy for the development of drug therapies for those infected with HIV.

Causes of Mutations

Mistakes in the process of DNA replication can crusade spontaneous mutations to occur. The mistake rate of DNA polymerase is i incorrect base per billion base pairs replicated. Exposure to mutagens can cause induced mutations, which are diverse types of chemical agents or radiation (Table \(\PageIndex{one}\)). Exposure to a mutagen can increase the charge per unit of mutation more than than 1000-fold. Mutagens are often as well carcinogens, agents that cause cancer. Notwithstanding, whereas nearly all carcinogens are mutagenic, not all mutagens are necessarily carcinogens.

Chemical Mutagens

Various types of chemic mutagens interact direct with Deoxyribonucleic acid either past acting as nucleoside analogs or past modifying nucleotide bases. Chemicals called nucleoside analogs are structurally like to normal nucleotide bases and can be incorporated into Dna during replication (Figure \(\PageIndex{3}\)). These base analogs induce mutations because they often have different base-pairing rules than the bases they supersede. Other chemical mutagens can modify normal DNA bases, resulting in different base-pairing rules. For example, nitrous acrid deaminates cytosine, converting it to uracil. Uracil then pairs with adenine in a subsequent circular of replication, resulting in the conversion of a GC base of operations pair to an AT base of operations pair. Nitrous acid also deaminates adenine to hypoxanthine, which base of operations pairs with cytosine instead of thymine, resulting in the conversion of a TA base of operations pair to a CG base pair.

Chemical mutagens known as intercalating amanuensisdue south work differently. These molecules slide between the stacked nitrogenous bases of the DNA double helix, distorting the molecule and creating atypical spacing between nucleotide base pairs (Effigy \(\PageIndex{4}\)). As a result, during DNA replication, Deoxyribonucleic acid polymerase may either skip replicating several nucleotides (creating a deletion) or insert extra nucleotides (creating an insertion). Either outcome may pb to a frameshift mutation. Combustion products like polycyclic effluvious hydrocarbons are peculiarly unsafe intercalating agents that tin lead to mutation-caused cancers. The intercalating agents ethidium bromide and acridine orange are commonly used in the laboratory to stain DNA for visualization and are potential mutagens.

Figure \(\PageIndex{3}\): (a) two-aminopurine nucleoside (2AP) structurally is a nucleoside analog to adenine nucleoside, whereas 5-bromouracil (5BU) is a nucleoside analog to thymine nucleoside. 2AP base pairs with C, converting an AT base pair to a GC base of operations pair subsequently several rounds of replication. 5BU pairs with G, converting an AT base pair to a GC base pair after several rounds of replication. (b) Nitrous acrid is a different type of chemical mutagen that modifies already existing nucleoside bases like C to produce U, which base pairs with A. This chemic modification, as shown here, results in converting a CG base pair to a TA base pair.

Figure \(\PageIndex{4}\): Intercalating agents, such as acridine, innovate atypical spacing betwixt base pairs, resulting in DNA polymerase introducing either a deletion or an insertion, leading to a potential frameshift mutation.

Radiation

Exposure to either ionizing or nonionizing radiation tin can each induce mutations in Dna, although by different mechanisms. Stiff ionizing radiations like X-rays and gamma rays can cause single- and double-stranded breaks in the DNA backbone through the formation of hydroxyl radicals on radiation exposure (Figure \(\PageIndex{5}\)). Ionizing radiations can also change bases; for example, the deamination of cytosine to uracil, analogous to the action of nitrous acrid.³ Ionizing radiations exposure is used to kill microbes to sterilize medical devices and foods, because of its dramatic nonspecific issue in damaging DNA, proteins, and other cellular components (see Using Concrete Methods to Control Microorganisms).

Nonionizing radiation, similar ultraviolet light, is not energetic enough to initiate these types of chemical changes. However, nonionizing radiation tin can induce dimer formation between two adjacent pyrimidine bases, ordinarily ii thymines, inside a nucleotide strand. During thymine dimer formation, the two adjacent thymines get covalently linked and, if left unrepaired, both Deoxyribonucleic acid replication and transcription are stalled at this indicate. DNA polymerase may proceed and replicate the dimer incorrectly, potentially leading to frameshift or point mutations.

Figure \(\PageIndex{v}\): (a) Ionizing radiations may atomic number 82 to the formation of unmarried-stranded and double-stranded breaks in the sugar-phosphate backbone of Deoxyribonucleic acid, as well as to the modification of bases (non shown). (b) Nonionizing radiation like ultraviolet lite can lead to the formation of thymine dimers, which can stall replication and transcription and introduce frameshift or indicate mutations.

Table \(\PageIndex{1}\): A Summary of Mutagenic Agents

Mutagenic Agents	Fashion of Action	Event on DNA	Resulting Type of Mutation
Nucleoside analogs
2-aminopurine	Is inserted in place of A but base of operations pairs with C	Converts AT to GC base pair	Indicate
v-bromouracil	Is inserted in place of T only base of operations pairs with G	Converts AT to GC base pair	Bespeak
Nucleotide-modifying agent
Nitrous oxide	Deaminates C to U	Converts GC to AT base of operations pair	Point
Intercalating agents
Acridine orange, ethidium bromide, polycyclic aromatic hydrocarbons	Distorts double helix, creates unusual spacing between nucleotides	Introduces small deletions and insertions	Frameshift
Ionizing radiations
X-rays, γ-rays	Forms hydroxyl radicals	Causes single- and double-strand Dna breaks	Repair mechanisms may introduce mutations
X-rays, γ-rays	Modifies bases (east.g., deaminating C to U)	Converts GC to AT base pair	Signal
Nonionizing radiation
Ultraviolet	Forms pyrimidine (unremarkably thymine) dimers	Causes Deoxyribonucleic acid replication errors	Frameshift or point

Exercise \(\PageIndex{3}\)

How does a base analog introduce a mutation?
How does an intercalating amanuensis innovate a mutation?
What type of mutagen causes thymine dimers?

Deoxyribonucleic acid Repair

The procedure of DNA replication is highly accurate, but mistakes tin occur spontaneously or be induced past mutagens. Uncorrected mistakes can lead to serious consequences for the phenotype. Cells take adult several repair mechanisms to minimize the number of mutations that persist.

Proofreading

Most of the mistakes introduced during Deoxyribonucleic acid replication are promptly corrected past most Deoxyribonucleic acid polymerases through a part called proofreading. In proofreading, the DNA polymerase reads the newly added base, ensuring that information technology is complementary to the corresponding base in the template strand before calculation the next ane. If an incorrect base has been added, the enzyme makes a cutting to release the wrong nucleotide and a new base is added.

Mismatch Repair

Some errors introduced during replication are corrected shortly after the replication mechanism has moved. This mechanism is chosen mismatch repair. The enzymes involved in this mechanism recognize the incorrectly added nucleotide, excise it, and replace it with the correct base. One example is the methyl-directed mismatch repair in E. coli. The DNA is hemimethylated. This means that the parental strand is methylated while the newly synthesized daughter strand is not. It takes several minutes before the new strand is methylated. Proteins MutS, MutL, and MutH bind to the hemimethylated site where the wrong nucleotide is constitute. MutH cuts the nonmethylated strand (the new strand). An exonuclease removes a portion of the strand (including the incorrect nucleotide). The gap formed is then filled in by Deoxyribonucleic acid pol 3 and ligase.

Repair of Thymine Dimers

Because the production of thymine dimers is common (many organisms cannot avoid ultraviolet low-cal), mechanisms have evolved to repair these lesions. In nucleotide excision repair (also called night repair), enzymes remove the pyrimidine dimer and replace it with the correct nucleotides (Figure \(\PageIndex{six}\)). In E. coli, the DNA is scanned past an enzyme complex. If a distortion in the double helix is found that was introduced by the pyrimidine dimer, the enzyme circuitous cuts the sugar-phosphate backbone several bases upstream and downstream of the dimer, and the segment of DNA between these two cuts is then enzymatically removed. Deoxyribonucleic acid political leader I replaces the missing nucleotides with the correct ones and DNA ligase seals the gap in the carbohydrate-phosphate backbone.

The directly repair (also called lite repair) of thymine dimers occurs through the process of photoreactivation in the presence of visible lite. An enzyme called photolyase recognizes the distortion in the DNA helix caused by the thymine dimer and binds to the dimer. Then, in the presence of visible light, the photolyase enzyme changes conformation and breaks autonomously the thymine dimer, allowing the thymines to once more correctly base pair with the adenines on the complementary strand. Photoreactivation appears to exist nowadays in all organisms, with the exception of placental mammals, including humans. Photoreactivation is especially important for organisms chronically exposed to ultraviolet radiation, like plants, photosynthetic bacteria, algae, and corals, to prevent the accumulation of mutations caused past thymine dimer germination.

Figure \(\PageIndex{half-dozen}\): Bacteria have two mechanisms for repairing thymine dimers. (a) In nucleotide excision repair, an enzyme complex recognizes the distortion in the DNA complex effectually the thymine dimer and cuts and removes the damaged Dna strand. The correct nucleotides are replaced by Dna pol I and the nucleotide strand is sealed by DNA ligase. (b) In photoreactivation, the enzyme photolyase binds to the thymine dimer and, in the presence of visible lite, breaks autonomously the dimer, restoring the base pairing of the thymines with complementary adenines on the opposite Dna strand.

Practise \(\PageIndex{four}\)

During mismatch repair, how does the enzyme recognize which is the new and which is the old strand?
How does an intercalating amanuensis introduce a mutation?
What blazon of mutation does photolyase repair?

Identifying Bacterial Mutants

I mutual technique used to place bacterial mutants is called replica plating. This technique is used to detect nutritional mutants, chosen auxotrophs, which have a mutation in a cistron encoding an enzyme in the biosynthesis pathway of a specific nutrient, such as an amino acid. As a result, whereas wild-blazon cells retain the power to grow normally on a medium defective the specific food, auxotrophs are unable to abound on such a medium. During replica plating (Figure \(\PageIndex{7}\)), a population of bacterial cells is mutagenized and so plated as individual cells on a complex nutritionally complete plate and allowed to grow into colonies. Cells from these colonies are removed from this master plate, oft using sterile velvet. This velvet, containing cells, is then pressed in the aforementioned orientation onto plates of various media. At least one plate should also be nutritionally consummate to ensure that cells are being properly transferred betwixt the plates. The other plates lack specific nutrients, allowing the researcher to discover various auxotrophic mutants unable to produce specific nutrients. Cells from the corresponding colony on the nutritionally complete plate can be used to recover the mutant for further written report.

Do \(\PageIndex{five}\)

Why are cells plated on a nutritionally complete plate in addition to nutrient-scarce plates when looking for a mutant?

The Ames Exam

The Ames test, developed by Bruce Ames (1928–) in the 1970s, is a method that uses bacteria for rapid, cheap screening of the carcinogenic potential of new chemic compounds. The test measures the mutation rate associated with exposure to the compound, which, if elevated, may indicate that exposure to this chemical compound is associated with greater cancer chance. The Ames exam uses as the examination organism a strain of Salmonella typhimurium that is a histidine auxotroph, unable to synthesize its own histidine because of a mutation in an essential gene required for its synthesis. Subsequently exposure to a potential mutagen, these bacteria are plated onto a medium defective histidine, and the number of mutants regaining the ability to synthesize histidine is recorded and compared with the number of such mutants that arise in the absence of the potential mutagen (Figure \(\PageIndex{8}\)). Chemicals that are more mutagenic volition bring about more mutants with restored histidine synthesis in the Ames exam. Because many chemicals are not directly mutagenic but are metabolized to mutagenic forms past liver enzymes, rat liver extract is commonly included at the showtime of this experiment to mimic liver metabolism. After the Ames test is conducted, compounds identified as mutagenic are farther tested for their potential carcinogenic backdrop by using other models, including beast models like mice and rats.

Effigy \(\PageIndex{vii}\): Identification of auxotrophic mutants, like histidine auxotrophs, is done using replica plating. After mutagenesis, colonies that grow on nutritionally complete medium merely not on medium lacking histidine are identified as histidine auxotrophs.

Figure \(\PageIndex{eight}\): The Ames test is used to identify mutagenic, potentially carcinogenic chemicals. A Salmonella histidine auxotroph is used as the test strain, exposed to a potential mutagen/carcinogen. The number of reversion mutants capable of growing in the absence of supplied histidine is counted and compared with the number of natural reversion mutants that arise in the absenteeism of the potential mutagen.

Do \(\PageIndex{6}\)

What mutation is used equally an indicator of mutation rate in the Ames exam?
Why can the Ames test piece of work as a test for carcinogenicity?

Key Concepts and Summary

A mutation is a heritable modify in Deoxyribonucleic acid. A mutation may lead to a change in the amino-acid sequence of a poly peptide, possibly affecting its role.
A point mutation affects a single base pair. A point mutation may crusade a silent mutation if the mRNA codon codes for the same amino acid, a missense mutation if the mRNA codon codes for a different amino acid, or a nonsense mutation if the mRNA codon becomes a stop codon.
Missense mutations may retain office, depending on the chemistry of the new amino acrid and its location in the protein. Nonsense mutations produce truncated and oftentimes nonfunctional proteins.
A frameshift mutation results from an insertion or deletion of a number of nucleotides that is not a multiple of three. The change in reading frame alters every amino acrid after the signal of the mutation and results in a nonfunctional protein.
Spontaneous mutations occur through DNA replication errors, whereas induced mutations occur through exposure to a mutagen.
Mutagenic agents are frequently carcinogenic merely not always. However, nearly all carcinogens are mutagenic.
Chemical mutagens include base analogs and chemicals that alter existing bases. In both cases, mutations are introduced later on several rounds of DNA replication.
Ionizing radiation, such as X-rays and γ-rays, leads to breakage of the phosphodiester backbone of Deoxyribonucleic acid and can also chemically modify bases to alter their base-pairing rules.
Nonionizing radiation similar ultraviolet light may introduce pyrimidine (thymine) dimers, which, during Dna replication and transcription, may introduce frameshift or bespeak mutations.
Cells have mechanisms to repair naturally occurring mutations. DNA polymerase has proofreading activity. Mismatch repair is a procedure to repair incorrectly incorporated bases afterwards DNA replication has been completed.
Pyrimidine dimers tin besides be repaired. In nucleotide excision repair (dark repair), enzymes recognize the distortion introduced past the pyrimidine dimer and replace the damaged strand with the correct bases, using the undamaged DNA strand as a template. Bacteria and other organisms may also use direct repair, in which the photolyase enzyme, in the presence of visible light, breaks autonomously the pyrimidines.
Through comparison of growth on the complete plate and lack of growth on media lacking specific nutrients, specific loss-of-function mutants called auxotrophs can be identified.
The Ames test is an inexpensive method that uses auxotrophic bacteria to measure mutagenicity of a chemical compound. Mutagenicity is an indicator of carcinogenic potential.

Multiple Option

Which of the following is a change in the sequence that leads to formation of a stop codon?

A. missense mutation
B. nonsense mutation
C. silent mutation
D. deletion mutation

The formation of pyrimidine dimers results from which of the following?

A. spontaneous errors past DNA polymerase
B. exposure to gamma radiation
C. exposure to ultraviolet radiation
D. exposure to intercalating agents

Which of the post-obit is an example of a frameshift mutation?

A. a deletion of a codon
B. missense mutation
C. silent mutation
D. deletion of one nucleotide

Which of the following is the blazon of DNA repair in which thymine dimers are straight cleaved down past the enzyme photolyase?

A. direct repair
B. nucleotide excision repair
C. mismatch repair
D. proofreading

Which of the following regarding the Ames examination is true?

A. Information technology is used to identify newly formed auxotrophic mutants.
B. It is used to place mutants with restored biosynthetic activity.
C. It is used to identify spontaneous mutants.
D. It is used to identify mutants lacking photoreactivation action.

Fill in the Blank

A chemical mutagen that is structurally similar to a nucleotide but has different base-pairing rules is called a ________.

nucleoside analog

The enzyme used in lite repair to split thymine dimers is called ________.

photolyase

The phenotype of an organism that is virtually commonly observed in nature is called the ________.

wild type

True/False

Carcinogens are typically mutagenic.

True

Brusk Reply

Why is information technology more likely that insertions or deletions will be more detrimental to a cell than bespeak mutations?

Critical Thinking

Below are several DNA sequences that are mutated compared with the wild-type sequence: 3'-T A C T Yard A C T Thou A C Thousand A T C-5'. Envision that each is a section of a Deoxyribonucleic acid molecule that has separated in grooming for transcription, so you are but seeing the template strand. Construct the complementary Deoxyribonucleic acid sequences (indicating five' and 3' ends) for each mutated DNA sequence, and then transcribe (indicating 5' and 3' ends) the template strands, and translate the mRNA molecules using the genetic code, recording the resulting amino acid sequence (indicating the Due north and C termini). What type of mutation is each?

Mutated DNA Template Strand #ane: iii'-T A C T G T C T G A C G A T C-5' Complementary Deoxyribonucleic acid sequence: mRNA sequence transcribed from template: Amino acrid sequence of peptide: Type of mutation:

Mutated DNA Template Strand #two: 3'-T A C Thou G A C T G A C K A T C-v' Complementary Dna sequence: mRNA sequence transcribed from template: Amino acid sequence of peptide: Type of mutation:

Mutated DNA Template Strand #3: 3'-T A C T G A C T G A C T A T C-v' Complementary Dna sequence: mRNA sequence transcribed from template: Amino acid sequence of peptide: Blazon of mutation:

Mutated Dna Template Strand #four: 3'-T A C Chiliad A C T G A C T A T C-5' Complementary Deoxyribonucleic acid sequence: mRNA sequence transcribed from template: Amino acid sequence of peptide: Type of mutation:

Why exercise you recollect the Ames exam is preferable to the use of animal models to screen chemical compounds for mutagenicity?

Footnotes

ane World Health Organization. " Global Health Observatory (GHO) Information, HIV/AIDS." http://world wide web.who.int/gho/hiv/en/. Accessed August 5, 2016.
2 World Wellness Organization. " Global Health Observatory (GHO) Data, HIV/AIDS." http://world wide web.who.int/gho/hiv/en/. Accessed August 5, 2016.
three K.R. Tindall et al. "Changes in DNA Base of operations Sequence Induced by Gamma-Ray Mutagenesis of Lambda Phage and Prophage." Genetics 118 no. 4 (1988):551–560.

Correspondent

Nina Parker, (Shenandoah Academy), Mark Schneegurt (Wichita State University), Anh-Hue Thi Tu (Georgia Southwestern State University), Philip Lister (Cardinal New Mexico Community College), and Brian Chiliad. Forster (Saint Joseph's Academy) with many contributing authors. Original content via Openstax (CC Past 4.0; Access for costless at https://openstax.org/books/microbiology/pages/1-introduction)

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