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I have been reading this article on drug resistance which explained that how random mutations in a bacterial colony can lead to development of drug resistance among some organisms in that colony.
A thought occurred to me that if mutations are just random (by random what I know (or think) here is the number and time of a mutation occurring in an organism in a normal environment may not be fixed but random) events arising from copy errors during DNA replications then how come some animals in nature mimic their surroundings to save themselves from predators or catch prey?
Let's consider for the time being that an animal exhibiting mimicry have evolved through natural selection, after suffering a mutation in their DNA which made them well adapted to their environment, and also saved them from their predators. Now we know a fit organism, in the struggle for existence, produces offsprings which can withstand the adversities of the surroundings and thus increases in numbers. In this way we may assume that due to many such helpful mutations led to the evolution of a new species.
This may sound simple but it actually seems to me as an over simplification of the events that lead to the development of 'that' new species. First of all not all mutations are helpful. Some are lethal as well. Also mutations may often be silent due to the degeneracy of the genetic code and presence of introns in the eukaryote. But let us consider here that the mutation suffered by our test organism was neither silent nor harmful, that too leaves us with infinite number of mutation possibilities to get a favourable organism from an unfit (to the surrounding in which our test organism is struggling) parent generation. Thus I think nature may not test each and every kind of possibility to select the fit one because in that case the test organisms will be far too many in number. Also if we consider that the fit one emerged just by chance out of million other possibilities then its sure that it was either too lucky or there is some other factor except 'just' mutation which can explain mimicry. Thus can only general mutation explain mimicry or we need something more to explain it?
/how come these animals (below) show such striking resemblance with their surroundings/
You are looking at the culmination of millions of generations of these insects. The mutations are random, but only the helpful ones (of all the random ones) produce an advantage for the organism and so persist in the species. If a random mutation caused an insect to look slightly more like its environment, that insect might do better at avoid predators or catching prey. Thus it would be more likely to produce offspring which would also have its mutation. Random mutations that caused an organism to look some other way would not confer any benefit as regards producing more offspring.
In each generation, if there is some random mutation that made the organism more similar to its environment, it could produce better fitness. The end result, over thousands (even millions) of years, is an organism which looks very much like its environment.
Fitness is what drives evolution. Read more at the link if you are interested. The more offspring I have the more I pass along my DNA and the better my fitness is. If I have a mutation that lets me have more offspring, that improves my genetic fitness.
Are mutations random?
I decided to open a new post (and directly attempt at answering it) as this claim is very common and a bit misleading. See Are mutations random?.
Your question does not need to be specific to species looking like their environment
You seem to not understand the basics of evolutionary biology. Your question is specific to why organisms look like their environment but what you should simply understand is the basics of evolution and selection.
You should definitely have a look at an intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for more information.
How can there be such striking similarities between some organisms and their environment?
Natural selection is the (main) answer.
An important reason (but definitely not the only one) for why a population of organisms would evolve to look like their surroundings is camouflage. Camouflaged organisms can typically have a higher fitness in a population that suffers from visual predators.
How can just random mutations explain mimicry? - Biology
Mutations can be beneficial, neutral, or harmful for the organism, but mutations do not "try" to supply what the organism "needs." Factors in the environment may influence the rate of mutation but are not generally thought to influence the direction of mutation. For example, exposure to harmful chemicals may increase the mutation rate, but will not cause more mutations that make the organism resistant to those chemicals. In this respect, mutations are random whether a particular mutation happens or not is unrelated to how useful that mutation would be.
For example, in the U.S. where people have access to shampoos with chemicals that kill lice, we have a lot of lice that are resistant to those chemicals. There are two possible explanations for this:
|Hypothesis A:||Hypothesis B:|
|Resistant strains of lice were always there and are just more frequent now because all the non-resistant lice died a sudsy death.||Exposure to lice shampoo actually caused mutations for resistance to the shampoo.|
Scientists generally think that the first explanation is the right one and that directed mutations, the second possible explanation relying on non-random mutation, is not correct.
Researchers have performed many experiments in this area. Though results can be interpreted in several ways, none unambiguously support directed mutation. Nevertheless, scientists are still doing research that provides evidence relevant to this issue.
In addition, experiments have made it clear that many mutations are in fact random, and did not occur because the organism was placed in a situation where the mutation would be useful. For example, if you expose bacteria to an antibiotic, you will likely observe an increased prevalence of antibiotic resistance. Esther and Joshua Lederberg determined that many of these mutations for antibiotic resistance existed in the population even before the population was exposed to the antibiotic and that exposure to the antibiotic did not cause those new resistant mutants to appear.
The Lederberg experiment
In 1952, Esther and Joshua Lederberg performed an experiment that helped show that many mutations are random, not directed. In this experiment, they capitalized on the ease with which bacteria can be grown and maintained. Bacteria grow into isolated colonies on plates. These colonies can be reproduced from an original plate to new plates by "stamping" the original plate with a cloth and then stamping empty plates with the same cloth. Bacteria from each colony are picked up on the cloth and then deposited on the new plates by the cloth.
Esther and Joshua hypothesized that antibiotic resistant strains of bacteria surviving an application of antibiotics had the resistance before their exposure to the antibiotics, not as a result of the exposure. Their experimental set-up is summarized below:
When the original plate is washed with penicillin, the same colonies (those in position X and Y) live even though these colonies on the original plate have never encountered penicillin before.
The Institute for Creation Research
"Enormous," "tremendous," "staggering"&mdashall these are adjectives used by geneticist Francisco Ayala to describe the amount of variation that can be expressed among the members of a single species. 1 Human beings, for example, range from very tall to very short, very dark to very light, soprano to bass, etc., etc. This tremendous amount of variation within species has been considered a challenge to creationists. Many ask: "How could the created progenitors of each kind possess enough variability among their genes to fill the earth with all the staggering diversity we see today and to refill it after a global flood only a few thousands years ago?"
If we use Ayalas figures, there would be no problem at all. He cites 6.7 % as the average proportion of human genes that show heterozygous allelic variation, e.g., straight vs. curly hair, Ss. On the basis of "only" 6.7 % heterozygosity, Ayala calculates that the average human couple could have 10 2017 children before they would have to have one child identical to another! That number, a one followed by 2017 zeroes, is greater than the number of sand grains by the sea, the number of stars in the sky, or the atoms in the known universe (a "mere" 10 80 )!
A single human couple could have been created with four alleles (two for each person) at each gene position (locus). Just two alleles for vocal cord characteristics, V and v, are responsible for the variation among tenor (VV), baritone (Vv), and bass (vv) singing voices in men, and hormone influences on development result in soprano (VV), mezzo-soprano (Vv), and alto voices (vv) as expressions of the same genes in women. Furthermore, several genes are known to exist in multiple copies, and some traits, like color, weight, and intelligence, depend on the cumulative effect of genes at two or more loci. Genes of each different copy and at each different locus could exist in four allelic forms, so the potential for diversity is staggering indeed!
Even more exciting is the recent discovery that some genes exist as protein coding segments of DNA separated by non-coding sequences called "introns." In addition to other functions, these introns may serve as "cross-over" points for "mixing and matching" subunits in the protein product. 2 If each subunit of such a gene existed in four allelic forms, consider the staggering amount of variation that one gene with three such subunits could produce! It is quite possible that such a clever&mdashand created&mdashmechanism is the means by which the information to produce millions of specific disease-fighting antibodies can be stored in only a few thousand genes.
Besides the positive contributors to genetic diversity described above, there is also one major negative contributor: megation. Believe it or not, orthodox evolutionists have tried to explain all the staggering variation both within and among species on the basis of these random changes in heredity called "mutations." What we know about mutations, however, makes them entirely unsuitable as any "raw materials for evolutionary progress."
As Ayala says, mutations in fruit flies have produced "extremely short wings, deformed bristles, blindness and other serious defects." Such mutations impose an increasingly heavy genetic burden or genetic load on a species. In her genetics textbook, Anna Pai makes it clear that "the word load is used intentionally to imply some sort of burden" that drags down the genetic quality of a species. 3 The list of human mutational disorders, or genetic diseases, for example, has already passed 1500, and it is continuing to grow.
By elimination of the unfit, natural selection reduces the harmful effects of mutations on a population, but it cannot solve the evolutionists genetic burden problem entirely. Most mutations are recessive. That is, like the hemophilia ("bleeder's disease") gene in England's Queen Victoria, the mutant can be carried, undetected by selection, in a person (or plant or animal) with a dominant gene that masks the mutant's effect.
Time, the usual "hero of the plot" for evolutionists, only makes genetic burden worse. As time goes on, existing mutants build up to a complex equilibrium point, and new mutations are continually occurring. That is why marriage among close relatives (e.g. Cain and his sister) posed no problem early in human history, even though now, thanks to the increase in mutational load with time, such marriages are considered most unwise. Already, 1% of all children born will require some professional help with genetic problems, and that percentage doubles in first-cousin marriages.
Genetic burden, then, becomes a staggering problem for evolutionists trying to explain the enormous adaptive variation within species on the basis of mutations. For any conceivable favorable mutation, a species must pay the price or bear the burden of more than 1000 harmful mutations of that gene. Against such a background of "genetic decay," any hypothetical favorable mutant in one gene would invariably be coupled to harmful changes in other genes. As mutational load increases with time, the survival of the species will be threatened as matings produce a greater percentage of offspring carrying serious genetic defects. 1,3
As the source of adaptive variability, then, mutations (and orthodox evolution theories) fail completely. As a source of "negative variability," however, mutations serve only too well. Basing their thinking on what we observe of mutations and their net effect (genetic burden), creationists use mutations to help explain the existence of disease, genetic defects, and other examples of "negative variation" within species.
Mutations are "pathologic" (disease-causing) and only "modify what pre-exists," as French zoologist Pierre-Paul Grassé says, so mutations have "no final evolutionary effect." 4 Instead, mutations point back to creation and to a corruption of the created order. There are 40-plus variants of hemoglobin, for example. All are variants of hemoglobin that points back to creation. All are less effective oxygen carriers than normal hemoglobin that points back to a corruption of the created order by time and chance.
At average mutation rates (one per million gene duplications), a human population of one billion would likely produce a thousand variant forms of hemoglobin. Lethal mutants would escape detection, and so would those that produced only minor changes, easily masked by a dominant normal gene. It is likely then, that the 40 or so recognized hemoglobin abnormalities represent only a small fraction of the genetic burden we bear at the hemoglobin position.
According to a new school of thought, "the neutral theory of molecular evolution," much of the staggering variation within species is due to mutations that are either neutral (without effect) or slightly deleterious. 5 Such a theory offers no comfort to the evolutionist trying to build grander life forms from mutations, but it is an expected consequence of the creation-corruption model. Interestingly, says Kimura, the amount of variation within species is too great for selection models of evolution, but too little for the neutral theory. He suggests that recent "genetic bottlenecks" have set back the "molecular clock" that otherwise ticks off mutations at a relatively constant rate. Scientists who recognize the fossil evidence of a recent global flood are not at all surprised, of course, that data suggest a recent "genetic bottleneck" which only a few of each kind survived!
Now, what about the time factor in the creation model? How long would it take, for example, to produce all the different shades of human skin color we have today?
There are several factors that contribute subtle tones to skin colors, but all people have the same basic skin coloring agent, the protein called melanin. We all have melanin skin color, just different amounts of it. (Not a very big difference, is it?) According to Davenport's study in the West Indies, the amount of skin color we have is influenced by at least two pairs of genes, A-a and B-b.
How long would it take AaBb parents to have children with all the variations in skin color we see today? Answer: one generation. Just one generation. As shown in the genetic square, one in 16 of the children of AaBb parents would likely have the darkest possible skin color (AABB) one brother or sister in 16 would likely have the lightest skin color (aabb) less than half (6/16) would be medium-skinned like their parents (any two "capital letter" genes) and one-quarter (4/16) would be a shade darker (3 capital letter genes) and a shade lighter (1 capital letter).
AaBb x AaBb
|AB|| AA |
What happened as the descendants of our first parents (and of Noah's family) multiplied over the earth? If those with very dark skin color (AABB) moved into the same area and/or chose to marry only those with very dark skin color, then all their children would be limited to very dark skin color. Similarly, children of parents with very light skin color (aabb) could have only very light skin, since their parents would have only "small a's and b's" to pass on. Parents with genotypes AAbb or aaBB would be limited to producing only children with medium-skin color. But where people of different backgrounds get back together again, as they do in the West Indies, then their children can once again express the full range of variation.
Except for mutational loss of skin color (albinism), then, the human gene pool would be the same now as it might have been at creation-just four genes, A, a, B, b, no more and no less. Actually, there are probably more gene loci and more alleles involved, which would make it even easier to store genetic variability in our created ancestors. As people multiplied over the earth (especially after Babel), the variation "hidden" in the genes of two average-looking parents came to visible expression in different tribes and tongues and nations.
The same would be true of the other created kinds as well: generalized ("average. looking") progenitors created with large and adaptable gene pools would break up into a variety of more specialized and adapted subtypes, as descendants of each created kind multiplied and filled the earth, both after creation and after the Flood.
There is new evidence that members of some species (including the famous peppered moth) may actually "choose" environments suitable for their trait combinations. 6 If "habitat choice" behavior were created (and did not have to originate by time, chance, and random mutations!), it would reduce the genetic burden that results when only one trait expression is "fittest," and it would also greatly accelerate the process of diversification within species.
Research and new discoveries have made it increasingly easy for creationists to account for phenomenal species diversification within short periods of time. These same discoveries have only magnified problems in orthodox neo-Darwinian thinking. It is encouraging, but not surprising, therefore, that an increasing number of students and professionals in science are accepting the creation model as the more logical inference from scientific observations and principles.
The scientist who is Christian can also look forward to the end of genetic burden, when the creation, now "subjected to futility" will be "set free from its bondage to decay, and obtain the glorious liberty of the children of God" (Romans 8).
* At time of publication, Dr. Gary E. Parker was a Research Associate in Bioscience at the Institute for Creation Research and taught Genetics and Biosystematics at Christian Heritage College, El Cajon CA. He is the senior author of several programmed instruction textbooks in biology.
Cite this article: Parker, G. 1980. Creation, Mutation, and Variation. Acts & Facts. 9 (11).
Biology note taking, Variation and Natural Selection. Questions.
-Genotype the information given by all the genes we have inside, and define our self.
Natural and Artificial Selection
- Natural Selection the greater chance of passing on genes by the best adapted organisms. The fitter organism is the one more likely to survive.
- Artificial Selection the choice by a farmerscientistpersongrower of only the “best” parents to breed, generation after generation. The humans intervene in the reproduction of other living organisms, and chose the characteristics they want the living organisms to have, and therefore, shape them as they like.
In the last class, Cecilia told us to read chapter 19 and make 7 or 10 questions about what we had read.
1- Which are the types of variation? Explain them.
2- Which is the name given to the chemical that can cause mutations?
3- What is the cause of the Down syndrome?
4- Give an example of an adaptive feature.
5- How can we describe evolution?
6- Name the ways in which genetic variation is produced.
7- Prepare a comparative chart detailing the differences between continuous and discontinuous variation.
RNA viruses versus DNA viruses
The Baltimore classification of viruses establishes the following categories according to the genetic material contained in the virion: positive-strand RNA viruses (e.g., rhinoviruses, hepatitis C virus, noroviruses, tobacco mosaic virus), negative-strand RNA viruses (influenza viruses, Ebola virus, rabies virus), double-strand RNA viruses (rotaviruses, bursal disease virus), retroviruses (HIV, human T cell leukemia virus), para-retroviruses (hepatitis B viruses), single-stranded DNA viruses (parvoviruses, bacteriophage ϕX174), and double-stranded DNA viruses (papillomaviruses, herpesviruses, adenoviruses, poxviruses). Viruses are the biological systems with the widest variation in mutation rates, the largest differences being found between RNA and DNA viruses. A summary of mutation rates for different viruses is provided in Table 1 . As discussed in previous work, the reliability of some of these rates is compromised by several sources of estimation error and bias . Despite these uncertainties, it can be inferred that viral mutation rates roughly range between 10 𢄨 and 10 𢄤 substitutions per nucleotide per cell infection (s/n/c), with DNA viruses occupying the 10 𢄨 𢄦 range and RNA viruses the 10 𢄦 𢄤 range (Fig. 2 a). These differences have several mechanistic bases. First, the polymerases of the vast majority of RNA viruses lack 3′ exonuclease proofreading activity and hence are more error-prone than those of DNA viruses [9, 10]. The exception to this rule is provided by coronaviruses, a family of positive-strand RNA viruses encoding a complex RNA-dependent RNA polymerase that has a 3′ exonuclease domain . Reverse transcriptases (RTs) also lack 3′ exonuclease activity [12, 13] and, hence, retroviruses (viruses with RNA-containing virions and a cellular DNA stage) and para-retroviruses (viruses with DNA-containing virions and a cellular RNA stage) mutate and evolve at rates similar to those of non-reverse transcribing RNA viruses (the latter are often called riboviruses).
Summary of viral mutation rates
|Class||Virus||Genome size (kb)||Average mutation rate (s/n/c) a||Individual estimates (s/n/c) b and references|
|ss(+)RNA||Bacteriophage Qβ c||4.22||1.4 ×ꀐ 𢄤||1.4 ×ꀐ 𢄤 |
|Tobacco mosaic virus||6.40||8.7 ×ꀐ 𢄦||8.7 ×ꀐ 𢄦 |
|Human rhinovirus 14||7.13||6.9 ×ꀐ 𢄥||4.8 ×ꀐ 𢄤 , 1.0 ×ꀐ 𢄥 |
|Poliovirus 1||7.44||9.0 ×ꀐ 𢄥||2.2 ×ꀐ 𢄥 [131, 132], 1.1 ×ꀐ 𢄤 , 3.0 ×ꀐ 𢄤 |
|Human norovirus G1||7.65||1.5 ×ꀐ 𢄤||1.5 ×ꀐ 𢄤 |
|Tobacco etch virus||9.49||1.2 ×ꀐ 𢄥||3.0 ×ꀐ 𢄥 , 4.8 ×ꀐ 𢄦 |
|Hepatitis C virus||9.65||3.8 ×ꀐ 𢄥||1.2 ×ꀐ 𢄤 , 2.5 ×ꀐ 𢄥 , 2.0 ×ꀐ 𢄥 , 3.5 ×ꀐ 𢄥 |
|Murine hepatitis virus||31.4||3.5 ×ꀐ 𢄦||3.5 ×ꀐ 𢄦 |
|ss(−)RNA||Vesicular stomatitis virus||11.2||3.7 ×ꀐ 𢄥||6.9 ×ꀐ 𢄥 [140, 141], 1.8 ×ꀐ 𢄥 , 4.2 ×ꀐ 𢄥 |
|Influenza A virus||13.6||2.5 ×ꀐ 𢄥||4.5 ×ꀐ 𢄥 , 7.1 ×ꀐ 𢄦 , 3.9 ×ꀐ 𢄥 , 3.1 ×ꀐ 𢄥 |
|Measles virus d||15.9||3.5 ×ꀐ 𢄥||2.8 ×ꀐ 𢄥 , 4.4 ×ꀐ 𢄥 |
|dsRNA||Bacteriophage 㩦||13.4||1.6 ×ꀐ 𢄦||1.6 ×ꀐ 𢄦 |
|Reverse transcribing||Duck hepatitis B virus||3.03||2.0 ×ꀐ 𢄥||2.0 ×ꀐ 𢄥 |
|Spleen necrosis virus||7.80||3.7 ×ꀐ 𢄥||2.4 ×ꀐ 𢄥 , 5.8 ×ꀐ 𢄥 |
|Murine leukemia virus||8.33||3.0 ×ꀐ 𢄥||6.0 ×ꀐ 𢄦 , 4.2 ×ꀐ 𢄥 , 1.1 ×ꀐ 𢄤 [155, 156]|
|Bovine leukemia virus||8.42||1.7 ×ꀐ 𢄥||1.7 ×ꀐ 𢄥 |
|Human T-cell leukemia virus||8.50||1.6 ×ꀐ 𢄥||1.6 ×ꀐ 𢄥 |
|HIV-1 (free virions)||9.18||6.3 ×ꀐ 𢄥||4.9 ×ꀐ 𢄥 [76, 159, 160], 1.0 ×ꀐ 𢄤 , 8.7 ×ꀐ 𢄥 , 4.4 ×ꀐ 𢄥 , 3.6 ×ꀐ 𢄥 , 9.3 ×ꀐ 𢄥 |
|HIV-1 (cellular DNA)||9.18||4.4 ×ꀐ 𢄣||4.4 ×ꀐ 𢄣 |
|Foamy virus||13.2||2.1 ×ꀐ 𢄥||2.1 ×ꀐ 𢄥 |
|Rous sarcoma virus||9.40||1.4 ×ꀐ 𢄤||1.4 ×ꀐ 𢄤 |
|ssDNA||Bacteriophage ΦX174||5.39||1.1 ×ꀐ 𢄦||1.3 ×ꀐ 𢄦 , 1.0 ×ꀐ 𢄦 |
|Bacteriophage m13||6.41||7.9 ×ꀐ 𢄧||7.9 ×ꀐ 𢄧 |
|dsDNA||Bacteriophage λ||48.5||5.4 ×ꀐ 𢄧||5.4 ×ꀐ 𢄧 [167, 168]|
|Herpes simplex virus||152||5.9 ×ꀐ 𢄨||5.9 ×ꀐ 𢄨 [169, 170]|
|Bacteriophage T2||169||9.8 ×ꀐ 𢄨||9.8 ×ꀐ 𢄨 [167, 171]|
|Human cytomegalovirus||235||2.0 ×ꀐ 𢄧||2.0 ×ꀐ 𢄧 |
a Geometric mean of the individual estimates
b Mutation rates were normalized to s/n/c units as detailed in previous work 
c This corresponds to a consensus estimate from several studies, see original publication for details
d Assuming linear replication, see original references for details
Mutation rate variation across viruses. a Range of variation of mutation rates for the seven Baltimore classes of viruses (ss single-strand, ds double-strand +/− genome polarity, RT retroviruses, pRT para-retroviruses). In the RT group, all mutation rates fall in the non-hatched arrow region except the HIV-1 mutation rate measured in cellular DNA, which is orders of magnitude higher than the rate measured in plasma. This is because many APOBEC-edited viral genomes fail to produce viable progeny and hence do not reach plasma (see text for details). b Negative correlation between genome size and mutation rate in viruses. Baltimore groups are indicated. The observed correlation can be explained in terms of differences between RNA and DNA viruses and between ss and ds viruses. In the RT group, the extremely high mutation rate of HIV-1 in cellular DNA is indicated with an arrow. In contrast, the HIV-1 mutation rate measured in plasma falls within the usual RT range
Whereas the dichotomy between RNA/RT and DNA viruses is well established from genetic and mechanistic standpoints, differences are less clear from the point of view of molecular evolution . Some DNA viruses have been shown to evolve at rates close to those of RNA viruses, including emerging canine parvovirus strains , human parvovirus , tomato yellow leaf curl geminivirus , beak-and-feather disease circovirus , and African swine fever virus (ASFV) , among others. This underscores the fact that evolution depends on multiple factors other than mutation rate, but also that mutation rates are unknown for many DNA viruses and may, in some cases, be higher than currently believed. Recent work with human cytomegalovirus has suggested a genome-wide average of 2 ×ꀐ 𢄧 s/n/c, a value slightly higher than previously thought for a large double-strand DNA virus , although this estimate was indirect. Since many DNA and RNA viruses share similar lifestyles, the question arises as to why mutation rates should have evolved so differently in these two broad groups.
Dept. of Clinical Cytogenetics, Addenbrookes Hospital/Science Photo Library/Getty Images Plus
Mutations can occur on genes located on sex chromosomes known as sex-linked genes. These genes on either the X chromosome or the Y chromosome determine the genetic characteristics of sex-linked traits. A gene mutation that occurs on the X chromosome can be dominant or recessive. X-linked dominant disorders are expressed in both males and females. X-linked recessive disorders are expressed in males and can be masked in females if the female's second X chromosome is normal. Y chromosome linked disorders are expressed only in males.
The Disadvantages of Chromosomal Mutations
Some mutations can be quite detrimental as well. The following are the some of the most common disadvantages of mutations in the chromosomes:
1. Genetic Disorder
2. Other Diseases
No matter what we do, the random changes in our genome are highly inevitable. And in this case, does the saying “the only constant is change” proves true?
How can just random mutations explain mimicry? - Biology
Since all cells in our body contain DNA, there are lots of places for mutations to occur however, some mutations cannot be passed on to offspring and do not matter for evolution. Somatic mutations occur in non-reproductive cells and won't be passed onto offspring. For example, the golden color on half of this Red Delicious apple was caused by a somatic mutation. Its seeds will not carry the mutation.
The only mutations that matter to large-scale evolution are those that can be passed on to offspring. These occur in reproductive cells like eggs and sperm and are called germ line mutations.
Effects of germ line mutations
A single germ line mutation can have a range of effects:
- No change occurs in phenotype.
Some mutations don't have any noticeable effect on the phenotype of an organism. This can happen in many situations: perhaps the mutation occurs in a stretch of DNA with no function, or perhaps the mutation occurs in a protein-coding region, but ends up not affecting the amino acid sequence of the protein.
Little mutations with big effects: Mutations to control genes
Mutations are often the victims of bad press unfairly stereotyped as unimportant or as a cause of genetic disease. While many mutations do indeed have small or negative effects, another sort of mutation gets less airtime. Mutations to control genes can have major (and sometimes positive) effects.
Some regions of DNA control other genes, determining when and where other genes are turned "on". Mutations in these parts of the genome can substantially change the way the organism is built. The difference between a mutation to a control gene and a mutation to a less powerful gene is a bit like the difference between whispering an instruction to the trumpet player in an orchestra versus whispering it to the orchestra's conductor. The impact of changing the conductor's behavior is much bigger and more coordinated than changing the behavior of an individual orchestra member. Similarly, a mutation in a gene "conductor" can cause a cascade of effects in the behavior of genes under its control.
Many organisms have powerful control genes that determine how the body is laid out. For example, Hox genes are found in many animals (including flies and humans) and designate where the head goes and which regions of the body grow appendages. Such master control genes help direct the building of body "units," such as segments, limbs, and eyes. So evolving a major change in basic body layout may not be so unlikely it may simply require a change in a Hox gene and the favor of natural selection.
Early approaches to mutagenesis relied on methods which produced entirely random mutations. In such methods, cells or organisms are exposed to mutagens such as UV radiation or mutagenic chemicals, and mutants with desired characteristics are then selected. Hermann Muller discovered in 1927 that X-rays can cause genetic mutations in fruit flies,  and went on to use the mutants he created for his studies in genetics.  For Escherichia coli, mutants may be selected first by exposure to UV radiation, then plated onto an agar medium. The colonies formed are then replica-plated, one in a rich medium, another in a minimal medium, and mutants that have specific nutritional requirements can then be identified by their inability to grow in the minimal medium. Similar procedures may be repeated with other types of cells and with different media for selection.
A number of methods for generating random mutations in specific proteins were later developed to screen for mutants with interesting or improved properties. These methods may involve the use of doped nucleotides in oligonucleotide synthesis, or conducting a PCR reaction in conditions that enhance misincorporation of nucleotides (error-prone PCR), for example by reducing the fidelity of replication or using nucleotide analogues.  A variation of this method for integrating non-biased mutations in a gene is sequence saturation mutagenesis.  PCR products which contain mutation(s) are then cloned into an expression vector and the mutant proteins produced can then be characterised.
In animal studies, alkylating agents such as N-ethyl-N-nitrosourea (ENU) have been used to generate mutant mice.   Ethyl methanesulfonate (EMS) is also often used to generate animal, plant, and virus mutants.   
In a European Union law (as 2001/18 directive), this kind of mutagenesis may be used to produce GMOs but the products are exempted from regulation: no labeling, no evaluation. 
Prior to the development site-directed mutagenesis techniques, all mutations made were random, and scientists had to use selection for the desired phenotype to find the desired mutation. Random mutagenesis techniques has an advantage in terms of how many mutations can be produced however, while random mutagenesis can produce a change in single nucleotides, it does not offer much control as to which nucleotide is being changed.  Many researchers therefore seek to introduce selected changes to DNA in a precise, site-specific manner. Early attempts uses analogs of nucleotides and other chemicals were first used to generate localized point mutations.  Such chemicals include aminopurine, which induces an AT to GC transition,  while nitrosoguanidine,  bisulfite,  and N 4 -hydroxycytidine may induce a GC to AT transition.   These techniques allow specific mutations to be engineered into a protein however, they are not flexible with respect to the kinds of mutants generated, nor are they as specific as later methods of site-directed mutagenesis and therefore have some degree of randomness. Other technologies such as cleavage of DNA at specific sites on the chromosome, addition of new nucleotides, and exchanging of base pairs it is now possible to decide where mutations can go.  
Current techniques for site-specific mutation originates from the primer extension technique developed in 1978. Such techniques commonly involve using pre-fabricated mutagenic oligonucleotides in a primer extension reaction with DNA polymerase. This methods allows for point mutation or deletion or insertion of small stretches of DNA at specific sites. Advances in methodology have made such mutagenesis now a relatively simple and efficient process. 
Newer and more efficient methods of site directed mutagenesis are being constantly developed. For example, a technique called "Seamless ligation cloning extract" (or SLiCE for short) allows for the cloning of certain sequences of DNA within the genome, and more than one DNA fragment can be inserted into the genome at once. 
Site directed mutagenesis allows the effect of specific mutation to be investigated. There are numerous uses for example, it has been used to determine how susceptible certain species were to chemicals that are often used In labs. The experiment used site directed mutagenesis to mimic the expected mutations of the specific chemical. The mutation resulted in a change in specific amino acids and the affects of this mutation were analyzed. 
The site-directed approach may be done systematically in such techniques as alanine scanning mutagenesis, whereby residues are systematically mutated to alanine in order to identify residues important to the structure or function of a protein.  Another comprehensive approach is site saturation mutagenesis where one codon or a set of codons may be substituted with all possible amino acids at the specific positions.  
Combinatorial mutagenesis is a site-directed protein engineering technique whereby multiple mutants of a protein can be simultaneously engineered based on analysis of the effects of additive individual mutations.  It provides a useful method to assess the combinatorial effect of a large number of mutations on protein function.  Large numbers of mutants may be screened for a particular characteristic by combinatorial analysis.  In this technique, multiple positions or short sequences along a DNA strand may be exhaustively modified to obtain a comprehensive library of mutant proteins.  The rate of incidence of beneficial variants can be improved by different methods for constructing mutagenesis libraries. One approach to this technique is to extract and replace a portion of the DNA sequence with a library of sequences containing all possible combinations at the desired mutation site. The content of the inserted segment can include sequences of structural significance, immunogenic property, or enzymatic function. A segment may also be inserted randomly into the gene in order to assess structural or functional significance of a particular part of a protein. 
The insertion of one or more base pairs, resulting in DNA mutations, is also known as insertional mutagenesis.  Engineered mutations such as these can provide important information in cancer research, such as mechanistic insights into the development of the disease. Retroviruses and transposons are the chief instrumental tools in insertional mutagenesis. Retroviruses, such as the mouse mammory tumor virus and murine leukemia virus, can be used to identify genes involved in carcinogenesis and understand the biological pathways of specific cancers.  Transposons, chromosomal segments that can undergo transposition, can be designed and applied to insertional mutagenesis as an instrument for cancer gene discovery.  These chromosomal segments allow insertional mutagenesis to be applied to virtually any tissue of choice while also allowing for more comprehensive, unbiased depth in DNA sequencing. 
Researchers have found four mechanisms of insertional mutagenesis that can be used on humans. the first mechanism is called enhancer insertion. Enhancers boost transcription of a particular gene by interacting with a promoter of that gene. This particular mechanism was first used to help severely immunocompromised patients I need of bone marrow. Gammaretroviruses carrying enhancers were then inserted into patients. The second mechanism is referred to as promoter insertion. Promoters provide our cells with the specific sequences needed to begin translation. Promoter insertion has helped researchers learn more about the HIV virus. The third mechanism is gene inactivation. An example of gene inactivation is using insertional mutagenesis to insert a retrovirus that disrupts the genome of the T cell in leukemia patients and giving them a specific antigen called CAR allowing the T cells to target cancer cells. The final mechanisms is referred to as mRNA 3' end substitution. Our genes occasionally undergo point mutations causing beta-thalassemia that interrupts red blood cell function. To fix this problem the correct gene sequence for the red blood cells are introduced and a substitution is made. 
Homologous recombination can be used to produce specific mutation in an organism. Vector containing DNA sequence similar to the gene to be modified is introduced to the cell, and by a process of recombination replaces the target gene in the chromosome. This method can be used to introduce a mutation or knock out a gene, for example as used in the production of knockout mice. 
Since 2013, the development of CRISPR-Cas9 technology has allowed for the efficient introduction of different types of mutations into the genome of a wide variety of organisms. The method does not require a transposon insertion site, leaves no marker, and its efficiency and simplicity has made it the preferred method for genome editing.  
As the cost of DNA oligonucleotide synthesis falls, artificial synthesis of a complete gene is now a viable method for introducing mutations into a gene. This method allows for extensive mutation at multiple sites, including the complete redesign of the codon usage of a gene to optimise it for a particular organism. 
The Causes of Genetic Mutations
In Summary: DNA Mutations
DNA polymerase can make mistakes while adding nucleotides. Most mistakes are corrected, but if they are not, they may result in a mutation defined as a permanent change in the DNA sequence. Mutations can be of many types, such as substitution, deletion, insertion, and translocation. Mutations in repair genes may lead to serious consequences such as cancer. Mutations can be induced or may occur spontaneously.