18.5: Mutation and Evolution - Biology

18.5: Mutation and Evolution - Biology

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Mutations are the raw materials of evolution. Evolution absolutely depends on mutations because this is the only way that new alleles and new regulatory regions are created. However, this seems paradoxical because most mutations that we observe are harmful (e.g., many missense mutations) or, at best, neutral, For example, "silent" mutations encoding the same amino acid. Also, many of the mutations in the vast amounts of DNA that lie between genes. Morevoer, most mutations in genes affect a single protein product (or a small set of related proteins produced by alternative splicing of a single gene transcript) while much evolutionary change involves myriad structural and functional changes in the phenotype.

So how can the small changes in genes caused by mutations, especially single-base substitutions ("point mutations"), lead to the large changes that distinguish one species from another? These questions have, as yet, only tentative answers.

One Solution: Duplication of Genes and Genomes

Mutations that would be harmful in a single pair of genes can be tolerated if those genes have first been duplicated. Gene duplication in a diploid organism provides a second pair of genes so that one pair can be safely mutated and tested in various combinations while the essential functions of the parent pair are kept intact.

Possible benefits:

  • Over time, one of the duplicates can acquire a new function. This can provide the basis for adaptive evolution.
  • But even while two paralogous genes are still similar in sequence and function, their existence provides redundancy ("belt and suspenders"). This may be a major reason why knocking out genes in yeast, "knockout mice", etc. so often has such a mild effect on the phenotype. The function of the knocked out gene can be taken over by a paralog.
  • After gene duplication, random loss of these genes at a later time in one group of descendants different from the loss in another group could provide a barrier (a "post-zygotic isolating mechanism") to their interbreeding. Such a barrier could cause speciation: the evolution of two different species from a single ancestral species.


  • Paralogous genes. Genes in one species that have arisen by duplication of an ancestral gene. Example: genes encoding olfactory receptors.
  • Duplication of the entire genome. Examples:
    • Polyploid angiosperms.
    • Genome analysis of three ascomycetes show that early in the evolution of the budding yeast, Saccharomyces cerevisiae, its entire genome was duplicated. Each chromosome of the other ascomycetes contains stretches of genes whose orthologs are distributed over two Saccharomyces cerevisiae chromosomes.
    • There is also evidence that vertebrate evolution has involved at least two duplications of the entire genome. Example: both the invertebrate Drosophila and the invertebrate chordate Amphioxus contain a single HOX gene cluster while mice and humans have four.

A Second Solution: Mutations in Regulatory Regions

Not all genes are expressed in all cells. In which cells and when a given gene will be expressed is controlled by the interaction of (1) extracellular signals turning on (or off),(2) transcription factors, which turn on (or off), and (3) particular genes. A mutation that would be lethal in the protein coding region of a gene need not be if it occurs in a control region (e.g. promoters and/or enhancers) of that gene. In fact, there is increasing evidence that mutations in control regions have played an important part in evolution. Examples:

  • Humans have a gene (LCT) encoding lactase; the enzyme that digests lactose (e.g. in milk). In most of the world's people, LCT is active in young children but is turned off in adults. However, northern Europeans and three different tribes of African pastoralists, for whom milk remains a part of the adult diet, carry a mutation in the control region of their lactase gene that permits it to be expressed in adults. The mutation is different in each of the 4 cases examples of convergent evolution.
  • There are very few differences in the coding sequences between genes of humans and chimpanzees. However, many of their shared genes differ in their control regions.
  • The story of Prx1. Prx1 encodes a transcription factor that is essential for forelimb growth in mammals. When mice have the enhancer region of their Prx1 replaced with the enhancer region of Prx1 from a bat (whose front limbs are wings), the front legs of resulting mice are 6% longer than normal. Here, then is a morphological change not driven by a change in the Prx1 protein but by a change in the expression of its gene.
  • The story of Pitx1
  • The story of Style2.1 in the domestic tomato

A Third Solution?

Another theoretically-possible way by which a point mutation might give rise to a new gene is if the point mutation in a previously noncoding section of DNA converts a triplet of nucleotides into ATG thus creating a new open reading frame (ORF). It is increasingly evident that much of noncoding DNA is transcribed into a heterogeneous collection of RNAs. Transcription of DNA with its newly-acquired ATG codon would produce an RNA molecule with a translation start codon (AUG). Translation of this RNA would create a protein that most likely would be useless, perhaps even harmful but might, on rare occasions, provide the starting point for the acquisition of a new useful gene.

Large Changes in Phenotype can come from small changes in Genotype

Selector Genes

The building of an organ requires the coordinated activity of many genes. However, these are often organized in hierarchies so that "upstream genes" regulate the activity of "downstream genes". The closer you get to the top with a mutation, the greater the changes affected downstream.

Follow these links to see examples of the influence of "master" (selector) genes on the phenotype.

  • Embryonic Development: Getting Started (especially the story of bicoid and nanos)
  • Organizing the Embryo: The Central Nervous System Organizing the Embryo: Segmentation (more on bicoid and nanos)
  • Embryonic Development: Putting on the finishing touches (especially the discussion of homeobox genes)

The Story of Pitx1

Pitx1 is homeobox gene (similar to bicoid in Drosophila) with orthologs found in all vertebrates. It contains 3 exons that encode a protein of some 283 amino acids (varying slightly in different species) which is a transcription factor that regulates the expression of other genes involved in the differentiation and function of multiple features including:

  1. the anterior lobe of the pituitary gland (Pitx1 = "Pituitary homeobox1");
  2. jaw development (mutations are associated with cleft palate);
  3. development of the thymus and some types of mechanoreceptors;
  4. development of the hind limbs.

Its activity in these regions is controlled by regulatory regions (promoters and/or enhancers) specific to each region (and presumably turned on by other transcription factors in the cells of those regions).

Pitx1 is an essential gene. Mutations in the coding regions are lethal when homozygous (shown in mice). However, mutations in noncoding regions need not be. All vertebrates have a pelvic girdle with associated bones which make up the pelvic fins of fishes and the hind legs of the tetrapods. Pitx1 is needed by them all for the proper development of these structures (as well as the other functions of Pitx1).

In a remarkable study of three-spined sticklebacks published in the 15 April 2004 issue of Nature, Michael Shapiro, Melissa Marks, Catherine Peichel, and their colleagues report that a mutation in a noncoding region of the Pitx1 gene accounts for most of the difference in the structure of the pelvic bones of the marine stickleback and its close freshwater cousins.

The marine sticklebacks have prominent spines jutting out in their pelvic region (red arrow) as well as the spines along the back (that give the fish its name). These spines may help protect them from being eaten by predators. (Drawing courtesy of the Parks Administration in the Emilia-Romagna region of Italy.) The also express the Pitx1 gene in various tissues, including thymus, mechanoreceptors, and the pelvic region.

The four species of stickleback that inhabit the Atlantic coast of North America. These species are sympatric between Newfoundland, Canada and Long Island, New York, United States. Image used iwth permission (CC BY-SA 3.0; Ghegeman).

The freshwater sticklebacks have no — or very much smaller — spines in their pelvic region. They express the identical Pitx1 gene in all the same tissues except those that develop into the pelvic structures. The reason: a mutation in an enhancer upstream of the Pitx1 exons. The unmutated enhancer turns on Pitx1 in the developing pelvic area. (Mice homozygous for a mutation in this control region have deformed hind limbs.)

Here then is a remarkable demonstration of how a single gene mutation can not only be viable but can lead to a major change in phenotype - adaptive evolution. (The changes seem not to have produce true speciation as yet. The marine and freshwater forms can interbreed. In fact, that is how the differences in their hind limbs were found to be primarily due to the expression of Pitx1.)

A survey of 21 different populations of sticklebacks - both freshwater and marine - from different regions of North America, Europe, and Japan has revealed a pattern of consistent genetic differences that distinguish the freshwater from the marine forms. However, only 17% of the distinguishing mutations were found in exons that alter the amino acid sequence of the encoded proteins. All the rest were "silent" and most, 41% or more, of these occurred in intergenic regions. These results further demonstrate the importance of mutations in regulatory regions - promoters and enhancers - in the evolution of adaptive phenotypes.

How are gene variants involved in evolution?

Evolution is the process by which populations of organisms change over generations. Genetic variations underlie these changes. Genetic variations can arise from gene variants (often called mutations) or from a normal process in which genetic material is rearranged as a cell is getting ready to divide (known as genetic recombination). Genetic variations that alter gene activity or protein function can introduce different traits in an organism. If a trait is advantageous and helps the individual survive and reproduce, the genetic variation is more likely to be passed to the next generation (a process known as natural selection). Over time, as generations of individuals with the trait continue to reproduce, the advantageous trait becomes increasingly common in a population, making the population different than an ancestral one. Sometimes the population becomes so different that it is considered a new species.

Not all variants influence evolution. Only hereditary variants, which occur in egg or sperm cells, can be passed to future generations and potentially contribute to evolution. Some variants occur during a person’s lifetime in only some of the body’s cells and are not hereditary, so natural selection cannot play a role. Also, many genetic changes have no impact on the function of a gene or protein and are not helpful or harmful. In addition, the environment in which a population of organisms lives is integral to the selection of traits. Some differences introduced by variants may help an organism survive in one setting but not in another—for example, resistance to a certain bacteria is only advantageous if that bacteria is found in a particular location and harms those who live there.

So why do some harmful traits, like genetic diseases, persist in populations instead of being removed by natural selection? There are several possible explanations, but in many cases, the answer is not clear. For some conditions, such as the neurological condition Huntington disease, signs and symptoms occur later in life, typically after a person has children, so the gene variant can be passed on despite being harmful. For other harmful traits, a phenomenon called reduced penetrance, in which some individuals with a disease-associated variant do not show signs and symptoms of the condition, can also allow harmful genetic variations to be passed to future generations. For some conditions, having one altered copy of a gene in each cell is advantageous, while having two altered copies causes disease. The best-studied example of this phenomenon is sickle cell disease: Having two altered copies of the HBB gene in each cell results in the disease, but having only one copy provides some resistance to malaria. This disease resistance helps explain why the variants that cause sickle cell disease are still found in many populations, especially in areas where malaria is prevalent.


Comparative genomic approaches have been used to identify sites where mutations are under purifying selection and of functional consequence by searching for sequences that are conserved across distantly related species. However, the performance of these approaches has not been rigorously evaluated under population genetic models. Further, short-lived functional elements may not leave a footprint of sequence conservation across many species. We use simulations to study how one measure of conservation, the Genomic Evolutionary Rate Profiling (GERP) score, relates to the strength of selection (Nes). We show that the GERP score is related to the strength of purifying selection. However, changes in selection coefficients or functional elements over time (i.e. functional turnover) can strongly affect the GERP distribution, leading to unexpected relationships between GERP and Nes. Further, we show that for functional elements that have a high turnover rate, adding more species to the analysis does not necessarily increase statistical power. Finally, we use the distribution of GERP scores across the human genome to compare models with and without turnover of sites where mutations are under purifying selection. We show that mutations in 4.51% of the noncoding human genome are under purifying selection and that most of this sequence has likely experienced changes in selection coefficients throughout mammalian evolution. Our work reveals limitations to using comparative genomic approaches to identify deleterious mutations. Commonly used GERP score thresholds miss over half of the noncoding sites in the human genome where mutations are under purifying selection.

What Is Natural Selection?

Natural selection is the process by which biological evolutionary changes take place. Natural selection acts on populations and not individuals. It is based on the following concepts:

  • Individuals in a population have different traits that can be inherited.
  • These individuals produce more young than the environment can support.
  • The individuals in a population that are best suited to their environment will leave more offspring, resulting in a change in the genetic makeup of a population.

The genetic variations that arise in a population happen by chance, but the process of natural selection does not. Natural selection is the result of the interactions between genetic variations in a population and the environment.

The environment determines which variations are more favorable. Individuals that possess traits that are better suited to their environment will survive to produce more offspring than other individuals. More favorable traits are thereby passed on to the population as a whole.

Coronavirus disease (COVID-19): Virus Evolution

When a virus replicates or makes copies of itself, it sometimes changes a little bit. These changes are called &ldquomutations.&rdquo A virus with one or several new mutations is referred to as a &ldquovariant&rdquo of the original virus.

The more viruses circulate, the more they may change. These changes can occasionally result in a virus variant that is better adapted to its environment compared to the original virus. This process of changing and selection of successful variants is called &ldquovirus evolution.&rdquo

Some mutations can lead to changes in a virus&rsquos characteristics, such as altered transmission (for example, it may spread more easily) or severity (for example, it may cause more severe disease).

Some viruses change quickly and others more slowly. SARS-CoV-2, the virus which causes COVID-19, tends to change more slowly than others such as HIV or influenza viruses. This could in part be explained by the virus&rsquos internal &ldquoproofreading mechanism&rdquo which can correct &ldquomistakes&rdquo when it makes copies of itself. Scientists continue to study this mechanism to better understand how it works.

It is normal for viruses to change, but it is still something scientists follow closely because there can be important implications. All viruses, including SARS-CoV-2, the virus that causes COVID-19, change over time. So far hundreds of variations of this virus have been identified worldwide. WHO and partners have been following them closely since January 2020.

Most changes have little to no impact on the virus&rsquo properties. However, depending on where the changes are located in the virus&rsquos genetic material, they may affect the virus&rsquos properties, such as transmission (for example, it may spread more easily) or severity (for example, it may cause more severe disease).

WHO and its international network of experts, are monitoring changes to the virus so that if significant mutations are identified, WHO can report any modifications to interventions needed by countries and individuals to prevent the spread of that variant. The current strategies and measures recommended by WHO continue to work against virus variants identified since the start of the pandemic.

The best way to limit and suppress the transmission of COVID-19 is for people to continue taking the necessary precautions to keep themselves and others safe.

Since the start of the outbreak, WHO has been working with a global network of expert laboratories around the world to support testing and better understanding of SARS-CoV-2, the virus that causes COVID-19.

Research groups have sequenced SARS-CoV-2 and shared these on public databases, including GISAID. This global collaboration allows scientists to better track the virus and how it is changing.

WHO&rsquos global SARS-CoV-2 laboratory network includes a dedicated SARS-CoV-2 Virus Evolution Working Group, which aims to detect new mutations quickly and assess their possible impact.

WHO recommends that all countries increase the sequencing of SARS-CoV-2 viruses where possible and share sequence data internationally to help one another monitor and respond to the evolving pandemic.

SARS-CoV-2 spreads primarily through human-to-human transmission, but there is evidence of transmission between humans and animals. Several animals like mink, dogs, domestic cats, lions, tigers and raccoon dogs have tested positive for SARS-CoV-2 after contact with infected humans.

There have been reports of large animal outbreaks in mink farms in several countries. SARS-CoV-2 can change while infecting minks. It has been observed that these mink variants are able to transmit back into humans through close contact with the mink. Preliminary results suggest that the mink variants infecting humans appear to have the same properties as other variants of the SARS-CoV-2 virus.

Further research is needed to better understand whether these mink variants will cause sustained transmission among humans and could have a negative impact on countermeasures, such as vaccines.

WHO works closely with other organizations, such as the Food and Agriculture Organization of the United Nations, and the World Organisation for Animal Health, to evaluate situations of SARS-CoV-2 in animals and transmission occurring between animals and humans.

Cultural Evolution Not the Same as Biological Evolution

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Evolution may take place at many different scales — and it may work differently in every one.

In biology, for instance, mutation and selection take place at the level of genes and organisms. But while cultural evolution also occurs at the individual level, the unit of selection — behavior — seems more susceptible to drastic change than a gene.

"In cultural evolution, small mutation rates are not the right choice," said Arne Traulsen, an evolutionary game theorist at the Max Planck Institute for Evolutionary Biology.

In a paper published Monday in the Proceedings of the National Academy of Sciences, Traulsen and colleagues modeled the effects of mutational variance in a standard game-theory model where individuals can be part of a community, steal from that community, or punish the thieves.

Most models of behavioral evolution, said Traulsen, assume that individuals will imitate their successful neighbors, with a minor allowance made for random variation — the cultural equivalent of heredity with minor mutations.

But in reality, people are unpredictable, prone to whimsical explorations and rash, seemingly irrational decisions. And when Traulsen reduced imitation and increased randomness, his simulations produced different end-states, with cooperation finally triumphing over thievery.

These results are not important to predicting human behavior, said
Traulsen, but underscore the importance of selection parameters to outcomes in the still-embryonic science of cultural evolution.

"Genetic evolution as we see it in biology is only one aspect of evolution," he said. "Taking a genetic approach and putting it onto cultural evolution and saying the mathematics are the same is not smart."

But the field is still so ambiguous and sketchily understood — entomologist Paul Ehrlich's chronicling of Polynesian canoe designs was the first rigorous description of cultural evolution — that Traulsen's conclusions are highly tentative.

"It's possible that the mechanisms might differ, but it's just a gut feeling," said Manfred Milinski, a Max Planck Institute evolutionary biologist and cooperation theorist who was not involved in the research. "This is a great area, which will be harvested in coming years. There are many people who think that most of our behavior has come about from cultural evolution." **

Citation: "Exploration dynamics in evolutionary games." By Arne Traulsen, Christoph Hauert, Hannelore Brandt, Martin A. Nowak, and Karl Sigmund. Proceedings of the National Academy of Sciences, Jan. 5, 2009.

In Human Evolution, Changes in Skin’s Barrier Set Northern Europeans Apart

The popular idea that Northern Europeans developed light skin to absorb more UV light so they could make more vitamin D – vital for healthy bones and immune function – is questioned by UC San Francisco researchers in a new study published online in the journal Evolutionary Biology.

Ramping up the skin’s capacity to capture UV light to make vitamin D is indeed important, according to a team led by Peter Elias, MD, a UCSF professor of dermatology. However, Elias and colleagues concluded in their study that changes in the skin’s function as a barrier to the elements made a greater contribution than alterations in skin pigment in the ability of Northern Europeans to make vitamin D.

Elias’ team concluded that genetic mutations compromising the skin’s ability to serve as a barrier allowed fair-skinned Northern Europeans to populate latitudes where too little ultraviolet B (UVB) light for vitamin D production penetrates the atmosphere.

Among scientists studying human evolution, it has been almost universally assumed that the need to make more vitamin D at Northern latitudes drove genetic mutations that reduce production of the pigment melanin, the main determinant of skin tone, according to Elias.

“At the higher latitudes of Great Britain, Scandinavia and the Baltic States, as well as Northern Germany and France, very little UVB light reaches the Earth, and it’s the key wavelength required by the skin for vitamin D generation,” Elias said.

“While it seems logical that the loss of the pigment melanin would serve as a compensatory mechanism, allowing for more irradiation of the skin surface and therefore more vitamin D production, this hypothesis is flawed for many reasons,” he continued. “For example, recent studies show that dark-skinned humans make vitamin D after sun exposure as efficiently as lightly-pigmented humans, and osteoporosis – which can be a sign of vitamin D deficiency – is less common, rather than more common, in darkly-pigmented humans.”

Furthermore, evidence for a south to north gradient in the prevalence of melanin mutations is weaker than for this alternative explanation explored by Elias and colleagues.

In earlier research, Elias began studying the role of skin as a barrier to water loss. He recently has focused on a specific skin-barrier protein called filaggrin, which is broken down into a molecule called urocanic acid – the most potent absorber of UVB light in the skin, according to Elias. “It’s certainly more important than melanin in lightly-pigmented skin,” he said.

In their new study, the researchers identified a strikingly higher prevalence of inborn mutations in the filaggrin gene among Northern European populations. Up to 10 percent of normal individuals carried mutations in the filaggrin gene in these northern nations, in contrast to much lower mutation rates in southern European, Asian and African populations.

Moreover, higher filaggrin mutation rates, which result in a loss of urocanic acid, correlated with higher vitamin D levels in the blood. Latitude-dependent variations in melanin genes are not similarly associated with vitamin D levels, according to Elias. This evidence suggests that changes in the skin barrier played a role in Northern European’s evolutionary adaptation to Northern latitudes, the study concluded.

Yet, there was an evolutionary tradeoff for these barrier-weakening filaggrin mutations, Elias said. Mutation bearers have a tendency for very dry skin, and are vulnerable to atopic dermatitis, asthma and food allergies. But these diseases have appeared only recently, and did not become a problem until humans began to live in densely populated urban environments, Elias said.

The Elias lab has shown that pigmented skin provides a better skin barrier, which he says was critically important for protection against dehydration and infections among ancestral humans living in sub-Saharan Africa. But the need for pigment to provide this extra protection waned as modern human populations migrated northward over the past 60,000 years or so, Elias said, while the need to absorb UVB light became greater, particularly for those humans who migrated to the far North behind retreating glaciers less than 10,000 years ago.

The data from the new study do not explain why Northern Europeans lost melanin. If the need to make more vitamin D did not drive pigment loss, what did? Elias speculates that, “Once human populations migrated northward, away from the tropical onslaught of UVB, pigment was gradually lost in service of metabolic conservation. The body will not waste precious energy and proteins to make proteins that it no longer needs.”

For the Evolutionary Biology study, labeled a “synthesis paper” by the journal, Elias and co-author Jacob P. Thyssen, MD, a professor at the University of Copenhagen, mapped the mutation data and measured the correlations with blood levels of vitamin D. Labs throughout the world identified the mutations. Daniel Bikle, MD, PhD, a UCSF professor of medicine, provided expertise on vitamin D metabolism.

The research was funded by the San Francisco Veterans Affairs Medical Center, the Department of Defense, the National Institutes of Health, and by a Lundbeck Foundation grant.

UCSF is the nation’s leading university exclusively focused on health. Now celebrating the 150th anniversary of its founding as a medical college, UCSF is dedicated to transforming health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy a graduate division with world-renowned programs in the biological sciences, a preeminent biomedical research enterprise and two top-tier hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco.

Coronavirus variants and mutations: The science explained

All viruses naturally mutate over time, and Sars-CoV-2 is no exception.

Since the virus was first identified a year ago, thousands of mutations have arisen.

The vast majority of mutations are "passengers" and will have little impact, says Dr Lucy van Dorp, an expert in the evolution of pathogens at University College London.

"They don't change the behaviour of the virus, they are just carried along."

But every once in a while, a virus strikes lucky by mutating in a way that helps it survive and reproduce.

"Viruses carrying these mutations can then increase in frequency due to natural selection, given the right epidemiological settings," Dr van Dorp says.

This is what seems to be happening with the variant that has spread across the UK, known as 202012/01, and a similar, but different variant, recently identified in South Africa (501.V2).

There is no evidence so far that either causes more severe disease, but the worry is that health systems will be overwhelmed by a rapid rise in cases.

In a rapid risk assessment of these "variants of concern", the European Centre for Disease Prevention and Control said they place increased pressure on health systems.

"Although there is no information that infections with these strains are more severe, due to increased transmissibility, the impact of Covid-19 disease in terms of hospitalisations and deaths is assessed as high, particularly for those in older age groups or with co-morbidities," the EU agency said.

The variants have different origins but share a mutation in a gene that encodes the spike protein, which the virus uses to latch on to and enter human cells.

Scientists think this could be why they appear more infectious.

"The UK and South African virus variants have changes in the spike gene consistent with the possibility that they are more infectious," says Prof Lawrence Young at the University of Warwick.

But as Dr Jeff Barrett, director of the Covid-19 genomics initiative at the Wellcome Sanger Institute in Hinxton, UK, points out, it's the combination of what the virus is doing and what we're doing that determines how fast it spreads.

"With the new variant, the situation changes more quickly as restrictions are relaxed and tightened, and there is less room for error in controlling the spread," he says.

"We don't have any evidence, however, that the new variant can fundamentally evade masks, social distancing, or the other interventions - we just need to apply them more strictly."

With vaccine roll-out underway, scientists are racing to understand the repercussions for vaccines, which are based on the spike protein sequence.

There is particular concern about the South Africa variant, which has several changes in the spike (S) protein.

Most experts think vaccines will still be effective, at least in the short term.

Dr Julian W Tang, a virologist at the University of Leicester, says vaccines can be modified to be "more close-fitting and effective against this variant in a few months".

"Meanwhile, most of us believe that the existing vaccines are likely to work to some extent to reduce infection/ transmission rates and severe disease against both the UK and South African variants - as the various mutations have not altered the S protein shape that the current vaccine-induced antibodies will not bind at all."

Scientists are carrying out laboratory studies to find out more about the variants. And they are tracking every move of the virus as it hopscotches around the world.

By taking a swab from an infected patient, the genetic code of the virus can be extracted and amplified before being "read" using a sequencer.

The string of letters, or nucleotides, allows genomes and mutations to be compared.

"It is thanks to these efforts, and UK testing laboratories, that the UK variant has been flagged so quickly as a potential cause of concern," Dr van Dorp says.

Prof Julian Hiscox, chair in infection and global health at the University of Liverpool, says that, through the efforts of scientists to sequence the virus, "we've got a really good handle on variants that emerge".

In the short-term, only the harshest of lockdowns will reduce case numbers, he says.

"What lockdown does is reduce the number of people with the virus and reduce the amount of virus out there and that's a good thing."

But in the long term, Prof Hiscox suspects, we may face a scenario like flu, where new vaccines are developed and administered every year.

"The problem is, the more variants we get, the greater the chance the virus will be able to escape part of the vaccine - and this may reduce [its] efficacy," he says.

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The Institute for Creation Research

ICR began publishing its popular free newsletter Acts & Facts in June 1972, over 31 years ago. The first two issues were 6-page, single-column, fold-over tract-like papers, black-and-white&mdashnot very impressive in appearance.

Issue No. 1 contained only news items describing some of our early campus meetings. Specially featured was the meeting held by Dr. Duane Gish on the Davis campus of the University of California. This was the meeting that involved an unscheduled 2½ hour debate with world-famous evolutionist, G. Ledyard Stebbins. A favorable response from the large student attendance and a very positive write-up in the student paper eventually led to Dr. Gish's famous cartoon booklet, Have You Been Brainwashed? which has been greatly used by the Lord in the past three decades, being distributed in the millions all over the world.

That issue also announced the publication of Dr. Gish's first book, Evolution: The Fossils Say No! which has been used widely and has won many evolutionists to accept the truth of special creation.

Issue No. 2 also was mostly news, but it did contain a semi-technical article on "The Mathematical Impossibility of Evolution" which is being reproduced herein as a matter of interest&mdashnot only of historical interest as the forerunner of our popular Impact articles (the first of which was published in the first 1973 issue), but also because it still seems to show in a very simple way that evolution is impossible&mdashno one, to my knowledge, has ever tried to refute it.

The third issue of Acts & Facts reported on the first ICR-sponsored expedition to Mount Ararat in search of Noah's Ark, led by John Morris. The first Impact article, however, was published in the January/February 1973 issue on the subject, "Evolution, Creation, and the Public Schools," urging that concerned citizens should use an educational and persuasion approach, rather than legislation or litigation, in trying to get a balanced approach to origins teaching accepted in the public schools.

In spite of this advice, however, many well-meaning creationists have tried&mdashalways unsuccessfully&mdashto try to force this issue. We still recommend education and persuasion as the best policy.

Anyway, an Impact article on significant scientific or apologetics topics has been published every month since that first 1973 Acts & Facts. The forerunner of all these, still quite valid, I believe, is reproduced with a few modifications below:

The Mathematical Impossibility of Evolution

According to the most-widely accepted theory of evolution today, the sole mechanism for producing evolution is that of random mutation combined with natural selection. Mutations are random changes in genetic systems. Natural selection is considered by evolutionists to be a sort of sieve, which retains the "good" mutations and allows the others to pass away.

Since random changes in ordered systems almost always will decrease the amount of order in those systems, nearly all mutations are harmful to the organisms which experience them. Nevertheless, the evolutionist insists that each complex organism in the world today has arisen by a long string of gradually accumulated good mutations preserved by natural selection. No one has ever actually observed a genuine mutation occurring in the natural environment which was beneficial (that is, adding useful genetic information to an existing genetic code), and therefore, retained by the selection process. For some reason, however, the idea has a certain persuasive quality about it and seems eminently reasonable to many people&mdashuntil it is examined quantitatively, that is!

For example, consider a very simple putative organism composed of only 200 integrated and functioning parts, and the problem of deriving that organism by this type of process. The system presumably must have started with only one part and then gradually built itself up over many generations into its 200-part organization. The developing organism, at each successive stage, must itself be integrated and functioning in its environment in order to survive until the next stage. Each successive stage, of course, becomes statistically less likely than the preceding one, since it is far easier for a complex system to break down than to build itself up. A four-component integrated system can more easily "mutate" (that is, somehow suddenly change) into a three-component system (or even a four-component non-functioning system) than into a five-component integrated system. If, at any step in the chain, the system mutates "downward," then it is either destroyed altogether or else moves backward, in an evolutionary sense.

Therefore, the successful production of a 200-component functioning organism requires, at least, 200 successive, successful such "mutations," each of which is highly unlikely. Even evolutionists recognize that true mutations are very rare, and beneficial mutations are extremely rare&mdashnot more than one out of a thousand mutations are beneficial, at the very most.

But let us give the evolutionist the benefit of every consideration. Assume that, at each mutational step, there is equally as much chance for it to be good as bad. Thus, the probability for the success of each mutation is assumed to be one out of two, or one-half. Elementary statistical theory shows that the probability of 200 successive mutations being successful is then (½) 200 , or one chance out of 10 60 . The number 10 60 , if written out, would be "one" followed by sixty "zeros." In other words, the chance that a 200-component organism could be formed by mutation and natural selection is less than one chance out of a trillion, trillion, trillion, trillion, trillion! Lest anyone think that a 200-part system is unreasonably complex, it should be noted that even a one-celled plant or animal may have millions of molecular "parts."

The evolutionist might react by saying that even though any one such mutating organism might not be successful, surely some around the world would be, especially in the 10 billion years (or 10 18 seconds) of assumed earth history. Therefore, let us imagine that every one of the earth's 10 14 square feet of surface harbors a billion (i.e., 10 9 ) mutating systems and that each mutation requires one-half second (actually it would take far more time than this). Each system can thus go through its 200 mutations in 100 seconds and then, if it is unsuccessful, start over for a new try. In 10 18 seconds, there can, therefore, be 10 18 /10 2 , or 10 16 , trials by each mutating system. Multiplying all these numbers together, there would be a total possible number of attempts to develop a 200-component system equal to 10 14 (10 9 ) (10 16 ), or 10 39 attempts. Since the probability against the success of any one of them is 10 60 , it is obvious that the probability that just one of these 10 39 attempts might be successful is only one out of 10 60 /10 39 , or 10 21 .

All this means that the chance that any kind of a 200-component integrated functioning organism could be developed by mutation and natural selection just once, anywhere in the world, in all the assumed expanse of geologic time, is less than one chance out of a billion trillion. What possible conclusion, therefore, can we derive from such considerations as this except that evolution by mutation and natural selection is mathematically and logically indefensible!


There have been many other ways in which creationist writers have used probability arguments to refute evolutionism, especially the idea of random changes preserved, if beneficial, by natural selection. James Coppedge devoted almost an entire book, Evolution: Possible or Impossible (Zondervan, 1973, 276 pp.), to this type of approach. I have also used other probability-type arguments to the same end (see, e.g., Science and Creation, Master Books, pp. 161-201).

The first such book, so far as I know, to use mathematics and probability in refuting evolution was written by a pastor, W. A. Williams, way back in 1928. Entitled, Evolution Disproved, it made a great impression on me when I first read it about 1943, at a time when I myself was still struggling with evolution.

In fact, evolutionists themselves have attacked traditional Darwinism on the same basis (see the Wistar Institute Symposium, Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution, 1967, 140 pp.). While these scientists did not reject evolution itself, they did insist that the Darwinian randomness postulate would never work.

Furthermore, since the law of increasing entropy, or the second law of thermodynamics, is essentially a statement of probabilities, many writers have also used that law itself to show that evolution on any significant scale is essentially impossible. Evolutionists have usually ignored the arguments or else used vacuous arguments against them ("Anything can happen given enough time" "The earth is an open system, so the second law doesn't apply" "Order can arise out of chaos through dissipative structures" etc.).

In the real world of scientific observation, as opposed to metaphysical speculation, however, no more complex system can ever "evolve" out of a less complex system, so the probability of the naturalistic origin of even the simplest imaginary form of life is zero.

The existence of complexity of any kind is evidence of God and creation. "Lift up your eyes on high, and behold who hath created these things, that bringeth out their host by number: He calleth them all by names by the greatness of His might, for that He is strong in power not one faileth" (Isaiah 40:26).

Watch the video: Population Genetics: When Darwin Met Mendel - Crash Course Biology #18 (May 2022).