Why are most of deleterious mutations recessive in nature? I understood that if it's recessive then one reason may be that the mutant gene doesn't code for a functional protein and so there is no phenotype to express. But why is it recessive in the first place?
It is a bit ironic that you phrase your question with 'in the first place'. There is a parsimonious explanation for the effect: Dominant deleterious variants are quickly removed by purifying selection whereas recessive deleterious variants can "hide" in individuals that carry a dominant neutral/advantageous variant.
You can think about it this way: In heterozygous carriers (in which the other variant has a neutral or positive fitness effect), a recessive deleterious variant has no (strong, depending on the dominance coefficient) negative effect on fitness and therefore, in those heterozygotes, purifying selection will not remove the variant (efficiently, again depending on the degree of dominance) - it can only act on homozygous carriers of the recessive variant. A consequence of that is that the recessive deleterious allele usually segregates at low frequency with most carriers being heterozygous.
In short: This probably has little to do with there being more recessive deleterious variants per se (even though that might also be the case due to the mechanisms you described in your question). In the snapshot we are looking at when we investigate genetic data, the likelihood of finding dominant deleterious alleles is way lower than finding recessive deleterious alleles as the latter usually just persist for a way longer period of time.
Why wouldn't a beneficial mutation be passed down to descendants?
Individuals are born with mana, which accounts for their life force and has a hand in determining the strength of their spells. Mana level and composition is determined by a person's genes, which they inherit from a mix of their parents. There are three factors that decide magical power:
Maximum reserve: This describes the level of reserves that a person contains. Individuals with extremely high mana reserves represent the strongest of witches, and can access the most powerful spells in mage craft. However, they have more difficulty in controlling and directing the flow of their mana. As a result, their spells take longer to perform. They also have a slow recharge rate, lengthening the time period between spells.
Focus rate: This describes the level of control a person has over their mana flow. Individuals high in this category have small reserves of mana, and can be considered weaker than average. However, they have much more control, allowing them to be more precise and direct. While those with high reserves are battering rams, they are a scalpel. They also have slow recharge rates, leading to longer intervals between spells.
Recharge rate: This is the category that most people fall into. They have average reserves of mana, as well as typical levels of control over it. They have a higher rate of recovery, allowing them to recharge their mana quicker than the other categories.
Very rarely, a person is born with high stats in all three sections. These individuals have large power levels with excellent control over their mana, as well as quick recharge rates. These individuals are considered the diamond in the rough, and are the most powerful and formidable mages in the world. The way evolution works, successful mutations are supposed to be inherited by descendants, as they allowed the parent organism to better survive and thrive compared to others of their race. As offspring becoming more successful, they eventually supplant others of their kind and become dominant. In the case of these badass mages however, their superiority only lasts once a generation. Their traits that make them powerful are not passed down to their offspring. Families who have instances of these mages often try pairing them in order to create a line of powerful offspring, but these are never successful in creating the desired outcome.
Why would this be the case?
Hidden burden: Most people carry recessive disease mutations
Humans carry an average of one to two mutations per person that can cause severe genetic disorders or prenatal death when two copies of the same mutation are inherited, according to estimates published today in the journal Genetics. The new numbers were made possible by a long-term collaboration between medical researchers and a unique community that has maintained detailed family histories for many generations.
"These records offered a fantastic opportunity to estimate disease mutation carrier rates in a new way that disentangles the effects of genetic and socioeconomic factors," said lead author Ziyue Gao of the University of Chicago.
Most genetic disorders that result in sterility or childhood death are caused by recessive mutations, DNA sequence variants that are harmless when a person carries only one copy. But if such mutations are present at both copies (where one copy was inherited from each parent), they can cause devastating diseases like cystic fibrosis.
Recessive disease mutations are much more common than those that are harmful even in a single copy, because such "dominant" mutations are more easily eliminated by natural selection. But exactly how common are the recessive disease-causing mutations in humans?
Previous efforts to estimate the number have relied on studies of disease in children born to related parents. In this method, the increased rates of childhood mortality and disease in these families are assumed to be due to recessive mutations. But this method mixes up the effects of genetics and socioeconomic factors.
For example, in some places, marriage between close relatives correlates with poverty. In those cases, children with related parents can have higher disease and death rates simply because their families suffer from poor nutrition or lack of access to medical care. "There are many different non-genetic factors that can bias this kind of approach," said Gao.
But the new method elegantly sidesteps this problem. It relies on the fact that the Hutterites, a religious community that settled in North America in the 1870s, keep meticulous genealogical records and live a communal lifestyle that ensures uniform access to healthcare and food.
Co-author Carole Ober of the University of Chicago has worked closely with a group of Hutterites from South Dakota for two decades, studying genetic contributions to disease using a large 13-generation family tree that traces the ancestry of more than 1,500 living people.
Molly Przeworski, a population geneticist at Columbia University, realized that this ancestry tree could be used to estimate the number of recessive disease mutations carried by the group's founders in the 18th and 19th century. This calculation was possible because Ober's team and other medical researchers had compiled comprehensive records on the frequency of disorders that cause sterility or childhood death in the study population.
Using this information, the team estimated that there were around three mutations of this type for every five people among the original founders. But that only counted mutations that allow children carrying two copies to survive at least until birth. Based on estimates of the proportion of recessive mutations that cause death during fetal development, the team concluded that each founder carried approximately one to two recessive mutations that cause sterility or death before adolescence.
"This number is probably lower than the real average for most populations, but it is in the right ballpark," said Gao. "Most importantly, unlike previous estimates, it is unaffected by socioeconomic factors."
Gao explained that isolated founder populations like those in the study are expected to carry fewer harmful recessive mutations than the general population, which is one of several reasons why we expect a slightly higher number than one to two mutations on average. This number also excludes recessive mutations carried on the sex chromosomes.
Gao cautions that the number of recessive disease mutations will vary from person to person, and the new number doesn't necessarily help predict a specific couple's risk for passing on a genetic disorder. She also points out that most infant mortality worldwide is caused by non-genetic factors like nutrition and infectious disease, rather than inherited disorders.
Surprisingly, the recessive disease mutation estimate for humans is similar to those from fruit fly and fish species, even though these organisms all have different total genome sizes. "We don't yet understand why the number of recessive lethal mutations might be relatively constant across distantly related organisms," said Gao. "It's an interesting evolutionary question for further research."
List of Recessive Genetic Disorders
Autosomal recessive disorders occur when there is an abnormality in a gene copy, donated by both parents. Parents who carry the gene, but themselves do not suffer from the condition are called carriers or ‘heterozygotes’. When the child that inherits both the abnormal gene copies from parents is called ‘homozygote’. Some of the disorders in humans are as follows:
One of the most commonly inherited gene disorders in Caucasians of northern European origins is cystic fibrosis (CF). It is caused by mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. This condition causes the person to secrete abnormal amounts of body fluids like sweat and mucus. The mucus starts affecting the internal organ functioning leading to chronic infections. It also affects the pancreas that leads to decrease in absorption of essential nutrients in the body. The life expectancy of this autosomal recessive disorder has improved considerably since the last few years. This is due to the advancement of medical science related to the management of this condition.
Sickle Cell Anemia
Sickle cell anemia (SC) is a blood disorder where the structure of hemoglobin is abnormal. Hemoglobin is a very important protein that helps in carrying oxygen from the lungs to each and very part of the body. In case of sickle-cell anemia, the shape of the hemoglobin turns to a crescent shape or sickle shape, instead of the normal round shape. This causes the red blood cells to be destroyed sooner than the normal red blood cells. Sickle cells survive for only 15 days, whereas normal RBCs live up to 120 days. Thus, the affected person regularly becomes anemic due to lack of red blood cells. It causes the affected person to suffer from frequent infections, severe pain in the arms, legs, back and stomach. It also makes them vulnerable to mild jaundice and development of gallstones, stroke and eye problems.
Tay-Sachs disease is a fatal disorder that causes death of the affected child by the age of 5 years. This condition leads to progressive degeneration of the central nervous system. The degeneration occurs due to absence of an enzyme called hexosaminidase A (hex A). If Hex A is not present in the body, it causes fatty substances to start building up on the nerve cells, especially in the brain. This condition starts occurring when the baby is still in the womb. However, the condition becomes apparent only after several months of birth. Till date, there is no cure found for treatment of Tay Sachs disease.
Gaucher’s disease is a genetic disease that causes accumulation of fatty substances in the cells and organs. This condition occurs due to deficiency of an enzyme called glucocerebrosidase. In absence of the enzyme, the fatty substances accumulate in the white blood cells, spleen, liver, kidneys, brain, lungs and bone marrow. Thus, it leads to skeletal disorders, enlarged spleen, neurological complications, anemia, low platelet count, etc. It affects about 1 in 100 people born in United States.
Phenylketonuria (PKU) is an autosomal recessive metabolic disorder. It occurs due to the abnormal coding of enzyme phenylalanine hydroxylase (PAH). This causes the enzyme to become nonfunctional and leads to accumulation of the amino acid phenylalanine.
These are some of the recessive genetic disorders that affect many children and adults around the world. Some other conditions include Mucopolysaccharidosis (MPS), Osteogenesis imperfecta, Fanconi anemia, Ehlers-Danlos syndrome. One should undergo genetic counseling, especially when either of the partner has a family history of genetic disease. This will help reduce the chances of the child developing the disease or becoming a carrier of the genetic disorder.
Lionel Van Maldergem , . Paul Deltenre , in Swaiman's Pediatric Neurology (Sixth Edition) , 2017
Autosomal Recessive Inheritance
ARNSHL is caused by mutations in a limited set of genes, including GJB2, SLC26A4, MYO15A, OTOF, CDH23, and TMC1. GJB2 mutations represent the most frequently reported cause of ARNSHL. Over 100 different mutations have been reported in this gene ( http://davinci.crg.es/deafness/index.php ). It is frequent in European countries close to the Mediterranean (up to 50% of ARNSHL cases). One is particularly prevalent in European populations because of a founder effect: 35delG.
Another common mutation is SLC26A4, which also is involved in a syndromic form of ARNSHL, Pendred syndrome, in which HL is accompanied by a thyroid goiter. However, as goiter usually appears later in life, or in some cases never appears, it is also considered an NSHL gene. An ARNSHL gene in which mutations are associated with a recognizable audiological phenotype is that encoding otoferlin (OTOF). Mutations in this audiological gene often result in prelingual, profound ARNSHL associated with an ANSD electrophysiological profile.
13 Answers 13
The chance of mutation is increased by eating other mutated plants and animals
The humans in this world are familiar with the mutations, recognize their source, and avoid it as much as possible. While some exposure to the pollution is unavoidable because it simply exists everywhere, it seems unlikely that any mutated crops would be harvested or mutated animals would be commonly hunted for food. Exposure to the pollution is minimized and so is the chance of mutation.
Animals on the other hand are not so discriminating. In fact, many carnivorous animals preferentially hunt prey that are injured or disfigured, and a mutated animal may appear to them to fit the criteria. As a result, animals will ingest the pollution as a major part of their diet rather than just through background exposure entire ecosystems could exist in otherwise low-pollution areas where pollution stored in the mutants is constantly recycled to make the mutant population much higher than would otherwise be expected.
Related to the idea that the pollution can be absorbed from food, biomagnification could result in carnivorous animals having a much higher chance of mutation than humans even when the ambient pollution has decreased substantially. The concept is that plants and animals low in the food chain absorb toxins in amounts too small to be dangerous, but the animal one step higher in the food chain will eat that animal in large quantities and end up with a more significant concentration. Eventually even a small ambient concentration of the toxin will be extremely harmful to apex predators. Applying this to your situation, humans that eat a mixture of primarily plants and herbivores won't have many steps for this accumulation to occur. Meanwhile ecosystems with longer food chains could have the same background pollution level while having a much higher frequency of mutation among the larger carnivores, and even slight increases in the background pollution level would have disproportionate increases in the mutation rate. A (potentially) desirable side-effect is that wild mutants are typically derived from large and dangerous predators, and in the rare case that the mutation is beneficial these "monsters" could be a major threat.
Finally, if the link of mutated monsters are more likely to produce mutated offspring is key, all the same logic applies except restricted to gestation. In mammals that means the higher pollution levels from their lifestyle is key around pregnancy, and as described above a pregnant mutant animal is more likely to be consuming pollution than a pregnant mutant human, while egg-laying species have the critical period shortly before laying the eggs (though I can't claim any real expertise in what goes into that process). Essentially the link would be that mutant animals are mostly caused by environmental factors that humans intentionally avoid, so if an animal is a mutant it is likely to stay in the same environment and future generations would have the same chances of mutating, while humans actively avoid causing mutations so even if one happens by rare chance their offspring still only has the same rare chance of mutating.
Are most genetic disorders recessive or dominant?
Recessive disease mutations are much more common than those that are harmful even in a single copy, because such "dominant" mutations are more easily eliminated by natural selection.
Secondly, why are dominant genetic disorders rare? A single abnormal gene on one of the first 22 nonsex (autosomal) chromosomes from either parent can cause an autosomal disorder. Dominant inheritance means an abnormal gene from one parent can cause disease. This happens even when the matching gene from the other parent is normal.
Also to know is, are dominant traits more common than recessive?
A widespread misconception is that traits due to dominant alleles are the most common in the population. While this is sometimes true, it is not always the case. For example, the allele for Huntington's Disease is dominant, while the allele for not developing this disorder is recessive.
Dominance is a relationship between two alleles of a gene and their associated phenotypes. A "dominant" allele is dominant to a particular allele of the same gene that can be inferred from the context, but it may be recessive to a third allele, and codominant to a fourth.
Why are most mutations recessive? - Biology
2. Recessive Alleles
3. Human Example
B. Lethal Alleles
2. Dominant vs. Recessive
3. Heterozygous Condition
4. Human Example
C. Human Genetic Diseases
1. Sickle Cell Anemia
2. Tay-Sachs Disease
3. Cystic Fibrosis
4. Huntington's Disease
D. Inborn Metabolic Errors
1. Definition - a rare, random and inheritable change in a cell's genetic material (DNA)
2. Recessive Alleles - most mutations produce recessive alleles (If they produced dominant alleles that resulted in fatality, the mutations would soon be eliminated from the population.)
3. Human Example:
a. Hemophilia = a genetic disorder where the blood does not clot properly a moderate cut can be life-threatening for a hemophiliac
b. Normal DNA --- Production of Functional Clotting Factor --- Normal Blood Clotting Ability
c. Mutated DNA --- Production of Nonfunctional Clotting Factor --- No Blood Clotting Ability
d. Possible Genotypes:
1) Homozygous Dominant - NN - Normal Clotting
2) Heterozygous - Nn - Normal Clotting
3) Homozygous Recessive - No Clotting
B. Lethal Alleles
1. Definition - a mutated allele that fails to code for the production of a functional protein that is vital for life
2. Dominant vs. Recessive:
a. Dominant Lethal Allele - Quickly eliminated from the population, because usually causes death before the individual can reproduce.
b. Recessive Lethal Allele - Will only cause death in the homozygous recessive condition.
3. Heterozygous Condition:
a. Carrier - an individual who is heterozygous for a lethal allele or an allele causing any genetic disease
1. These individuals are able to live and reproduce.
2. Carriers do not phenotypically express the genetic condition.
3. These individuals, however, can pass the lethal allele onto offspring.
b. The average human is heterozygous for 3-5 lethal alleles.
c. Partially explains problems associated with inbreeding.
4. Human Example:
a. Brachydactyly - a genetic condition in which the fingers are abnormally short in heterozygotes however, this condition is fatal during infancy to homozygous recessive individuals due to major skeletal defects
b. Marriage between Two Brachydactyl People:
F1 Genotypic Results: 1 BB : 2 Bb : 1 bb
F1 Phenotypic Results: 1 Normal Child
2 Brachydactyl Children
1 Infant Death
C. Human Genetic Diseases
1. Sickle Cell Anemia - genetic condition that is often lethal in the homozygous recessive condition
a. Involved gene codes for the production of hemoglobin, which is an oxygen-carrying protein found in red blood cells
b. The alleles involved are governed by Codominance.
c. Genotypes and Phenotypes Involved:
1) NN - Homozygous Dominant - Normal Blood Cells
2) Nn - Heterozygous Carrier - Both Normal and Sickled Red Blood Cells Produced - Nn Genotype Conveys Resistance to Malaria (a potentially fatal mosquito-borne illness prevalent in third world nations)
3) nn - Homozygous Recessive - Sickle Cell Anemia - 50% chance of death by age 20
2. Tay-Sachs Disease - genetic condition that is lethal to all homozygous recessive individuals by age four
a. Incurable Metabolic Disorder
b. Results in Brain Deterioration
c. 1 in every 30 people of East European Jewish descent are carriers of the Tay-Sach's recessive allele
3. Cystic Fibrosis - genetic condition that is lethal to all homozygous recessive individuals by age 30
a. Incurable disorder in which thick mucus accumulates in the lungs leading to constant and dangerous respiratory infections
b. Most common lethal allele in the United States' Caucasian Population
4. Huntington's Disease - genetic condition caused by a dominant lethal allele
a. This dominant allele is still present in the population because the disease does not affect individuals until after reproductive stage of life (40-50 years of age).
b. Symptoms include twitching and depression
c. Results in Brain Degeneration and death within five years of onset
D. Inborn Metabolic Errors
1. Definition - genetic defect caused by a mutation of a gene coding for proteins that function as enzymes in the body's metabolic pathways
2. Phenylketonuria - PKU - genetic condition in which individual lacks the enzyme to convert phenylalanine to tyrosine
a. Can result in mental retardation and brain damage without treatment.
b. All babies born in the United States are tested for PKU before leaving the hospital.
c. Treatment is following a special diet avoiding such things are nutrasweet and diet foods.
d. Warning labels are on food products containing phenylalanine to warn those with PKU.
3. Albinism - genetic condition in which individual lacks the enzyme to convert tyrosine to melanin, which is a skin pigment
a. True albinos have very little melanin.
b. White hair, very light skin, and red pupils result from this severe lack of pigmentation.
c. Albinos must be very careful of sun exposure.
To test your knowledge about Mutations and Diseases, click on the Mutation Questions Link at the top of this page. After you answer the questions, be sure to check your responses by clicking on the Mutation Answers Link .
Why haven't recessive genes faded away?
I was thinking that eventually recessive genes would fade away, leaving only dominant genes. Why hasn't this happened/is it happening?
Genes cannot be dominant or recessive, alleles are dominant or recessive.
That said, there are many things that keep recessive alleles present in populations:
Some recessive alleles are beneficial (they increase the fitness of individuals who carry them). This doesn't always mean that the recessive phenotype is beneficial - for example, having one recessive allele for the sickle-cell gene causes individuals to be resistant to malaria, increasing fitness of heterozygotes in environments where malaria is common. Having two recessive alleles means you have the sickle-cell phenotype and the health problems that go with it.
Geneticists describe this as "overdominance," meaning that the individuals with one dominant and one recessive allele actually have a more extreme phenotype than individuals with two dominant alleles. It's also commonly referred to as "hybrid vigor," which gets at the idea that it's often beneficial to merge the traits from two very different parents so that their offspring can tolerate or react to a wider range of environments.
2) The placement of genes on chromosomes influences how they are inherited. Genes that are located near each other are linked, meaning that inheriting the allele on chromosome 1 for one gene makes it likely you'll also inherit the allele on chromosome 1 for any nearby genes. This means that selection for an allele of a gene that impacts fitness can result in selection for certain alleles of the nearby genes as well. Any alleles of the nearby genes that are on the same chromosome as the beneficial allele of the gene undergoing selection will also be selected for, so recessive alleles can increase in frequency this way.
3) While it's simple to get rid of individuals with two copies of a recessive allele (especially if they have lowered fitness as a result), it's tricky to identify the individuals carrying recessive alleles that don't impact phenotype. This means that the alleles can stay latent in the population for a long time without necessarily producing any homozygous recessive individuals.
4) Most mutations result in formation of recessive alleles (instead of dominant ones) by causing the loss of function of a protein. Often what we consider to be the recessive allele of a gene may actually be many versions of a coding sequence (resulting from many different mutations) which all don't work. This means that new mutations are likely to be recessive, keeping the frequency high in the population.
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).