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Will a less favorable allele's frequency go to 0?

Will a less favorable allele's frequency go to 0?


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For example, a pond is dark in color. There are two alleles. The dark color allele is dominant over the light color one. Let's assume that the relative fitness of both the homozygous dominant and heterozygous is 1, and the relative fitness of the homozygous recessive is 0.5. When I ran the simulation, I changed no other values. My data after 251 generations is this: My question is that being homozygous recessive is clearly less favorable, and even though being homozygous dominant and heterozygous carry the same advantage instead of heterozygote advantage, why wouldn't the recessive allele disappear?


  • Natural selection increases or decreases biological traits within a population, thereby selecting for individuals with greater evolutionary fitness.
  • An individual with a high evolutionary fitness will provide more beneficial contributions to the gene pool of the next generation.
  • Relative fitness, which compares an organism&rsquos fitness to the others in the population, allows researchers to establish how a population may evolve by determining which individuals are contributing additional offspring to the next generation.
  • Stabilizing selection, directional selection, diversifying selection, frequency -dependent selection, and sexual selection all contribute to the way natural selection can affect variation within a population.
  • natural selection: a process in which individual organisms or phenotypes that possess favorable traits are more likely to survive and reproduce
  • fecundity: number, rate, or capacity of offspring production
  • Darwinian fitness: the average contribution to the gene pool of the next generation that is made by an average individual of the specified genotype or phenotype

Part 1 - &ldquoI&rsquom Looking Over&hellip&rdquo

White clover (Trifolium repens), a small perennial plant, is found throughout the world, and has two forms. One variant has entirely green leaves (plain) and the other has green leaves with a prominent white stripe (striped). Do an internet search for clover to see if you can readily identify each type.

Both variants of white clover (plain and striped) are found along the coast of Long Island, New York. Most of Long Island is only a few feet above sea level. A series of low grass-covered hills separated by shallow depressions covers the area behind the oceanfront dunes. The shallow depressions reach to the water table, so they tend to be permanently moist year round and do not freeze in winter. Water drains away quickly from the low hills, which tend to dry out many times over the year and freeze in the winter. The habitat in the shallow depressions is more hospitable to molluscs (snails and slugs) that feed on clover. One type of clover is more common in shallow depressions while the other type is more likely to be found on low hills. When organisms of the same group or species have different phenotypes, they are referred to as polymorphisms.

At the end of the case, we will come back to New York and ask you to predict which type of white clover is most abundant in each microhabitat.

1. Propose a reason why one type of clover might be found in the depressions and another type on the hills.

2. Provide another example of a polymorphism you have observed in an animal group.

3. Sketch the coast of Long Island as it is described in the paragraph above, showing the types of organism and landscape and where they can be found.

ESSENTIAL QUESTION: What type of clover is found in the depressions and what type of clover would be mostly likely found on the hills of Long Island?

On a larger scale, the two types of clovers are found in different frequencies. The chart (Fig 1) below shows the distribution of the clover in North Carolina and Minnesota. Table 1 describes the physical habitats of the two locations.

Figure 1: Relative frequency of white clover variants in Minnesota and North Carolina

Average Temperature (monthly)

Mean # of days with a high above 32° C

Mean # of days with a low below 0° C

Average Yearly Precipitation

Presence of herbivores (molluscs such as snails, slugs)

small population, not present in winter

large, active population, present all year

4. A habitat is defined as the place and conditions under which an organism lives. This includes physical factors such as temperature, soil type, availability of nutrients, moisture and the presence of other organisms.

  1. Which habitat is farther north?
  2. Which habitat is generally warmer?
  3. Which habitat has more rain?
  4. Which habitat has a greater presence of herbivores?

5. Which habitat has a greater distribution of white-striped clover? Suggest a reason for this based on the data in the table.


Allele Frequency

The allele frequency (or gene frequency) is the rate at which a specific allele appears within a population. In population genetics, the term evolution is defined as a change in the frequency of an allele in a population. Frequencies range from 0, present in no individuals, to 1, present in all individuals. The gene pool is the sum of all the alleles at all genes in a population.

Using the ABO blood type system as an example, the frequency of one of the alleles, for example I A , is the number of copies of that allele divided by all the copies of the ABO gene in the population, i.e. all the alleles. Allele frequencies can be expressed as a decimal or as a percent and always add up to 1, or 100 percent, of the total population. For example, in a sample population of humans, the frequency of the I A allele might be 0.26, which would mean that 26% of the chromosomes in that population carry the I A allele. If we also know that the frequency of the I B allele in this population is 0.14, then the frequency of the i allele is 0.6, which we obtain by subtracting all the known allele frequencies from 1 (thus: 1 &ndash 0.26 &ndash 0.14 = 0.6). A change in any of these allele frequencies over time would constitute evolution in the population.


Population Genetics

Recall that a gene for a particular character may have several variants, or alleles, that code for different traits associated with that character. For example, in the ABO blood type system in humans, three alleles determine the particular blood-type protein on the surface of red blood cells. Each individual in a population of diploid organisms can only carry two alleles for a particular gene, but more than two may be present in the individuals that make up the population. Mendel followed alleles as they were inherited from parent to offspring. In the early twentieth century, biologists began to study what happens to all the alleles in a population in a field of study known as population genetics.

Until now, we have defined evolution as a change in the characteristics of a population of organisms, but behind that phenotypic change is genetic change. In population genetic terms, evolution is defined as a change in the frequency of an allele in a population. Using the ABO system as an example, the frequency of one of the alleles, I A , is the number of copies of that allele divided by all the copies of the ABO gene in the population. For example, a study in Jordan found a frequency of I A to be 26.1 percent. 2 The I B , I 0 alleles made up 13.4 percent and 60.5 percent of the alleles respectively, and all of the frequencies add up to 100 percent. A change in this frequency over time would constitute evolution in the population.

There are several ways the allele frequencies of a population can change. One of those ways is natural selection. If a given allele confers a phenotype that allows an individual to have more offspring that survive and reproduce, that allele, by virtue of being inherited by those offspring, will be in greater frequency in the next generation. Since allele frequencies always add up to 100 percent, an increase in the frequency of one allele always means a corresponding decrease in one or more of the other alleles. Highly beneficial alleles may, over a very few generations, become &ldquofixed&rdquo in this way, meaning that every individual of the population will carry the allele. Similarly, detrimental alleles may be swiftly eliminated from the gene pool, the sum of all the alleles in a population. Part of the study of population genetics is tracking how selective forces change the allele frequencies in a population over time, which can give scientists clues regarding the selective forces that may be operating on a given population. The studies of changes in wing coloration in the peppered moth from mottled white to dark in response to soot-covered tree trunks and then back to mottled white when factories stopped producing so much soot is a classic example of studying evolution in natural populations (Figure (PageIndex<5>)).

Figure (PageIndex<5>): As the Industrial Revolution caused trees to darken from soot, darker colored peppered moths were better camouflaged than the lighter colored ones, which caused there to be more of the darker colored moths in the population.

In the early twentieth century, English mathematician Godfrey Hardy and German physician Wilhelm Weinberg independently provided an explanation for a somewhat counterintuitive concept. Hardy&rsquos original explanation was in response to a misunderstanding as to why a &ldquodominant&rdquo allele, one that masks a recessive allele, should not increase in frequency in a population until it eliminated all the other alleles. The question resulted from a common confusion about what &ldquodominant&rdquo means, but it forced Hardy, who was not even a biologist, to point out that if there are no factors that affect an allele frequency those frequencies will remain constant from one generation to the next. This principle is now known as the Hardy-Weinberg equilibrium. The theory states that a population&rsquos allele and genotype frequencies are inherently stable&mdashunless some kind of evolutionary force is acting on the population, the population would carry the same alleles in the same proportions generation after generation. Individuals would, as a whole, look essentially the same and this would be unrelated to whether the alleles were dominant or recessive. The four most important evolutionary forces, which will disrupt the equilibrium, are natural selection, mutation, genetic drift, and migration into or out of a population. A fifth factor, nonrandom mating, will also disrupt the Hardy-Weinberg equilibrium but only by shifting genotype frequencies, not allele frequencies. In nonrandom mating, individuals are more likely to mate with like individuals (or unlike individuals) rather than at random. Since nonrandom mating does not change allele frequencies, it does not cause evolution directly. Natural selection has been described. Mutation creates one allele out of another one and changes an allele&rsquos frequency by a small, but continuous amount each generation. Each allele is generated by a low, constant mutation rate that will slowly increase the allele&rsquos frequency in a population if no other forces act on the allele. If natural selection acts against the allele, it will be removed from the population at a low rate leading to a frequency that results from a balance between selection and mutation. This is one reason that genetic diseases remain in the human population at very low frequencies. If the allele is favored by selection, it will increase in frequency. Genetic drift causes random changes in allele frequencies when populations are small. Genetic drift can often be important in evolution, as discussed in the next section. Finally, if two populations of a species have different allele frequencies, migration of individuals between them will cause frequency changes in both populations. As it happens, there is no population in which one or more of these processes are not operating, so populations are always evolving, and the Hardy-Weinberg equilibrium will never be exactly observed. However, the Hardy-Weinberg principle gives scientists a baseline expectation for allele frequencies in a non-evolving population to which they can compare evolving populations and thereby infer what evolutionary forces might be at play. The population is evolving if the frequencies of alleles or genotypes deviate from the value expected from the Hardy-Weinberg principle.

Darwin identified a special case of natural selection that he called sexual selection. Sexual selection affects an individual&rsquos ability to mate and thus produce offspring, and it leads to the evolution of dramatic traits that often appear maladaptive in terms of survival but persist because they give their owners greater reproductive success. Sexual selection occurs in two ways: through male&ndashmale competition for mates and through female selection of mates. Male&ndashmale competition takes the form of conflicts between males, which are often ritualized, but may also pose significant threats to a male&rsquos survival. Sometimes the competition is for territory, with females more likely to mate with males with higher quality territories. Female choice occurs when females choose a male based on a particular trait, such as feather colors, the performance of a mating dance, or the building of an elaborate structure. In some cases male&ndashmale competition and female choice combine in the mating process. In each of these cases, the traits selected for, such as fighting ability or feather color and length, become enhanced in the males. In general, it is thought that sexual selection can proceed to a point at which natural selection against a character&rsquos further enhancement prevents its further evolution because it negatively impacts the male&rsquos ability to survive. For example, colorful feathers or an elaborate display make the male more obvious to predators.


Calculating Gene (Allele) Frequencies in a Population | Genetics

Application of Hardy-Weinberg law in calculating Gene (Allele) frequencies in a population.

The gene frequencies for the autosomal and sex-chromosomal allele can be determined by the help of Hardy-Weinberg law by the following method:

A. Calculation of Gene Frequencies of Autosomal Genes:

An autosomal gene locus may have codominant alleles, dominant and recessive alleles or multiple alleles. If one desires to determine the gene frequencies for each of these kinds of autosomal alleles in a given population, he has to adopt the different methods.

(i) Calculation of Gene Frequencies for Codominant Alleles:

When codominant alleles are present in a two-allele system, each genotype has a characteristic phenotype. The numbers of each allele in both homozygous and heterozygous conditions may be counted in a sample of individuals from the population and expressed as a percentage of total number of alleles in a sample.

If the sample is representative of the entire population (containing proportionately same numbers as found in the entire population) then we can obtain an estimate of the allelic frequencies in the gene pool. If in a given sample of N individuals of which D are homozygous for one allele (A 1 A 1 ), H are heterozygous (A 1 A 2 ), and R are homozygous for the allele (A 2 A 2 ), then N D + H + R.

Since each of the N individuals are diploid at this locus, there are 2N alleles represented in the sample. Each A 1 A 1 genotype has two A 1 alleles. Heterozygotes have only one A 1 allele. Letting p represents the frequency of the A 1 allele and q the frequency of the A 2 allele, we have-

The M-N blood type furnishes a useful example of a series of phenotypes due to a pair of codominant alleles. None of three possible phenotypes, M, MN and N, appears to have any selection value. The frequencies of the two alleles (viz., L M and L N ) for a sample from a group of white Americans living in New York City, Boston, and Columbus, Ohio, can be calculated by the following ways-

The sample of 6,129 Caucasian people includes the following three groups according to phenotypes and genotypes on M-N system:

To calculate frequencies of the two codominant alleles, L M and L N , it should be kept in mind that these 6,129 persons possess a total of 6,129 x 2 = 12,258 genes. The number of L M alleles, for example, is 1,787 + 1,787 + 3,039. Thus, calculation of the frequency of L M and L N alleles is worked out in this way.

Thus, the frequencies of the two codominant alleles in this sample are almost equal, and this is reflected in the close approximation to a 1: 2: 1 ratio, which is a simple monohybrid ratio for codominant alleles in Mendelian genetics.

Gene frequencies expressed as decimals may be used directly to state probabilities (a probability is a function that represents the likelihood of occurrence of any particular form of an event).

If we can assume this sample to be representative of the population, then there is a probability of 0.5395 that of the chromosomes bearing this pair of alleles, any one selected randomly will bear gene L M , and 0.4605 that it will bear L N .

Let p represents genotypic frequency of L M allele and q represents frequency of L N allele, then the frequencies of three genotypes to be expected in the population are as follows:

(ii) Calculation of Gene (Allele) Frequencies for Dominant and Recessive Autosomal Alleles:

Calculation of the gene frequencies for alleles which exhibit dominance and recessive relationships requires a different approach from that used with codominant alleles. A dominant phenotype may have either of two genotypes, AA or Aa, but we have no way (other than by laboriously test- crossing each dominant phenotype) of distinguishing how many are homozygous or heterozygous in our sample.

The only phenotype whose genotype is known for certain is the recessive (aa). If the population is in equilibrium then we can obtain an estimate of q (the frequency of the recessive allele) from q^ (the frequency of the recessive genotype or phenotype).

If 75% of a population was of the dominant phenotype (A-), then 25% would have recessive phenotype (aa). If the population is in equilibrium with respect to this gene locus, we expect q 2 = frequency of aa.

Then q 2 = 0.25, q = 0.5, p= 1 – q = 0.5.

An interesting pair of contrasting traits, which has been detected in human populations and has no known selective value is the ability or inability to taste the chemical phenylthiocarbamide (“PTC”, C7H3N2S), also called phenylthiourea. This was reported by Fox in 1932, who found a similar situation for several other thiocarbamides.

The test is a simple one which can easily be performed by any genetics class. The usual procedure is to impregnate filter paper with a dilute solution of PTC (about 0.5 to 1 gram per litre), allow it to dry, then place a bit of the treated paper on the tip of the tongue.

About 70 per cent of an American white population can taste the substance, generally as very bitter, rarely as sweetish. Although the physiological basis is unknown, tasting ability does depend on a completely dominant gene, which we will designate as T. Thus tasters are T-(TT or Tt) and nontasters are tt.

From a group of 146 genetics students who tested themselves for tasting ability, 105 were tasters and 41 were nontasters. From these results the frequencies of alleles T and t in the sample may be calculated readily.

The 41 (28 per cent of the sample) nontasters are persons of tt genotype, and in the Hardy-Weinberg theorem may be represented by q 2 Therefore:

q 2 = 0.28 and q = VO.28 = 0.53 (frequency of t).

Since p + q = 1, p = 1 – q p = 1 – 0.53 = 0.47 (frequency of T). The frequency of homozygous and heterozygous tasters may now be computed, using the expression p 2 + 2pq + q 2 = 1.

2pq = Tt = 2(0.47 x 0.53) = 0.4983

q 2 = tt = (0.53) 2 = 0.2809/1.0000

By testing representative samples of different populations, the frequencies of T and t in those groups may similarly be calculated.

(iii) Calculation of Gene (Allele) Frequencies for Autosomal Multiple Alleles:

The binomial (p + q) 2 = 1 applies when only two autosomal alleles occur at a given locus. For cases of multiple alleles we simply add more terms to the expression.

The four human blood types—A, B, AB, and O are determined by a series of three multiple alleles, L A or I A , L B or I B , and L 0 or i, if we neglect the various subtypes.

Hence, in a gene frequency analysis, we can here let:

Thus, genotypes in a population under random mating will be given by (p + q + r) 2 .

In a sample of 23,787 persons from Rechester, New York, following frequencies for four blood types were recorded:

The frequency of each allele may now be calculated from these data, remembering that we have let p, q and r represent the frequencies of genes I A , I B , i respectively.

The value of r, that is, the frequency of gene i, is immediately evident from the figure given:

r = √0.444 = 0.6663 (= frequency of i)

The sum of A and O phenotypes is given by (p + r) 2 = 0.418 + 0.444 = 0.862 therefore,

So p = (p + r)-r = 0.9284 – 0.6663 = 0.2621 (= frequency of I A ).

Because p + q +r= 1, q = 1 – (p + r) = 1 -0.9284 = 0.0716 (= frequency of I B ) we can now calculate genotypic frequencies as shown in the following table:

B. Calculation of Gene Frequencies for Sex-Linked Genes:

Alleles in the sex chromosomes may occur in a different frequency than those in autosomes because of the difficult arrangements of sex chromosomes in the two sexes. The same techniques with one small modification, may be used in treating sex-linked genes.

However, since human males or Drosophila males being heterogametic sexes contain only one X chromosome, they cannot reflect a binomial distribution for random combination of pairs of sex-linked genes as females. Equilibrium distribution of genotypes for a sex-linked trait, where p + q = I, is given by-

In human population red-green colour blindness is a trait due to a sex-linked recessive, which we may designate r. About 8 per cent of males are colour-blind. This shows at once that q, the frequency of gene r, is 0.08 and p, the frequency of its normal allele, R is 0.92. Thus, the frequency of colour blind females is expected to be q 2 = 0.0064.

This is about what is found. Sex-linked dominants may be handled in a similar fashion in the case of normal colour vision, with the value of p – 0.92, the incidence of normal women is p 2 + 2pq = 0.9936.


Introduction

RNA editing is a post-transcriptional mechanism that introduces differences between RNA and its corresponding DNA sequence [1]. One type of RNA editing events, the A-to-I editing, is catalyzed by adenosine deaminase acting on RNA (ADARs) acting on dsRNAs. Due to the prevalence of dsRNA structures formed by the inverted repeated Alus in primates, which are the preferred substrates of ADARs, A-to-I editing is the most common type of RNA editing in primates [2]. The recent next-generation sequencing technology dramatically accelerated the study of A-to-I editing regulation on a genome-wide scale [3,4,5,6], with nearly 3% of the human genome estimated to be subject to the regulation [4].

Most A-to-I RNA editing sites in primates are contributed by the expansion of primate-specific Alu elements [6, 7]. Of these widespread A-to-I RNA editing sites in primates, only a small proportion is located in well-recognized functional regions, such as the protein-coding or miRNA encoding loci, and presumably implicated in altering sequences of proteins or miRNAs [1, 3, 5, 8, 9]. As population genetics analyses have recently hinted at the functional relevance for editing sites in other genomic regions, functional dissection of these pervasive RNA editing sites has emerged as a critical issue in the field [5, 10,11,12]. While several recent studies have suggested the potential crosstalk between RNA editing and other regulatory processes, such as alternative splicing, piRNA biogenesis and cytosolic dsRNA response [10, 11, 13, 14], an in-depth functional perspective of the widespread A-to-I editing sites in primate evolution remain to be addressed.

Recently, a group of A-to-I RNA editing sites has been reported in candidate gene studies to be genomically encoded as non-editable nucleotide in other closely related species [15, 16], representing a recent birth or death process of RNA editing through DNA point mutations. Importantly, comprehensive characterization of this subset of RNA editome, if exists, could advance the evolutionary and functional interrogation of primate RNA editing regulation in the following regards. First, because RNA editing identification depends heavily on the quality and sequencing depth of the transcriptome, defining a species-specific editing site in a comparative transcriptome study could be confounded by multiple factors such as technical limitation in ascertaining true absence of editing from the failure of detection [17]. In contrast, a distinctive list of RNA editing gain or loss events through DNA point mutations constitutes a valuable alternative to confidently define newly originated, species-specific RNA editing events. This possibility is supported by the notions that the editing regulation in out-group species is explicitly absent (genomically encoded as non-editable nucleotides) and that the ancestral state of these sites could be inferred with sequence data of multiple reference species. This unique group of RNA editing events with evolutionary age may thus provide a basis for studying the evolutionary significance of RNA editing in primate evolution. Second, comparative genomics analyses of these RNA editing events could also provide functional connection of RNA editing to particular gene regulatory processes. As the editing sites detected in one species were genomically encoded as non-editable nucleotides in the other species, a cross-species comparison of the outcome of a gene regulatory level may provide clues to the functional implications of these species-specific editing sites, which would further illuminate the general functions of RNA editing regulation.

Although cases of the birth or death process of RNA editing through DNA point mutation have been reported, the generality of this phenomenon on a genome-wide scale, the models underpinning the phenomenon, and the applications of these events in evolutionary and functional interrogation of RNA editing regulation remain largely unresolved. In particular, this phenomenon on the population level, in which the A-to-I RNA editing sites detected in some individuals are genomically encoded as non-editable nucleotides in other individuals, would complement these analyses. However, this type of polymorphic editing sites is intentionally omitted primarily due to the potential false positives of these events and their consequent removal by the editing-calling computational pipelines [4, 18,19,20].


Background

Domestication is a special mode of evolution. Extensive studies have been carried out to understand the domestication process and genes associated with morphological changes [1,2,3,4]. Meanwhile, genomes also went through profound changes during domestication. Recent studies documented the base-composition difference and mutation rate difference between populations separated by either domestication or demographic bottleneck event, which provide novel insights on genome evolution [5,6,7]. Further investigation in DNA base composition, mutation spectrum, and the potential relationship between them is necessary to advance our understanding of genome changes.

DNA base composition is an essential genomic feature. Remarkable research progress has been made in several areas, including codon usage bias [8], isochore structure [9, 10], and GC-biased gene conversion [11]. Recently, a conserved base-composition pattern, modern accessions having significantly higher [A] and [T] values across genome-wide polymorphic sites than accessions sampled from their wild relatives, was discovered with natural populations across multiple species [5]. Different genomic regions exhibit different patterns of a number of genomic features such as DNA methylation, GC content, and recombination rate [12,13,14,15]. It would be interesting to study the regional variation of genome change pattern, captured by base composition summarized from polymorphic sites.

Mutation is a fundamental factor that generates the genetic variation upon which selection, drift, and recombination act. Point mutations are the most common type of mutations with a universal bias toward high AT, primarily due to the high rate of transition mutations [16]. Recent studies indicated that mutation rate can be different across populations [6, 7]. Divergence in mutation rates or types between populations are one of several factors that affect genetic variation patterns [17]. Analysis of data from multiple mutation accumulation experiments, either accumulating spontaneous or induced mutations, demonstrated higher [AT] values across mutation sites in derived lines at the end of mutation experiments than in ancestral lines, which suggested that base-composition difference can emerge from mutation sites [5]. Characterization of mutation spectrum in natural populations may help unravel the mechanism of genome change [18].

Organisms have evolved a complex system to monitor and repair DNA damage caused by various exogenous mutagens, such as solar-ultraviolet (UV) radiation, reactive oxygen species, excess boron or aluminum, and pathogenic microorganisms [19]. For plants, solar-UV radiation is a major exogenous mutagen as they use sunlight for photosynthesis. The primary solar UV-induced DNA lesion, cyclobutane pyrimidine dimers (CPDs), induces C→T base transitions [20]. CPDs distort the DNA’s double-helix structure, which influences DNA unwinding and DNA replication, and ultimately affect cell cycle [21]. Using sets of SNPs private to different human populations, a recent study suggested that UV might have been involved in the mutation spectrum change [6].

DNA methylation is a major form of epigenetic modification in many eukaryotic genomes. It not only regulates gene expression and silences transposons and repeat sequences, but also affects mutation rates [22,23,24,25]. DNA methylation occurs in CG, CHG (where H = A, C, or T), and CHH sequence contexts in plants [26, 27]. The relative frequency of DNA methylation varies substantially along chromosome. DNA methylation is primarily distributed in the heterochromatin regions that are mostly composed of tandem repeats and transposons [12, 13, 28]. It has been shown that methylation of cytosine residue at CpG sites can enhance the solar UV-promoted CPD formation [25]. We can ask whether the rate of solar UV-induced mutations varies along the chromosome and whether base composition can summarize such variation.

In this study, we report findings from the analysis of millions of SNPs segregating among 100 accessions from a teosinte-maize comparison set and among 302 accessions from a wild-domesticated soybean comparison set. First, we show that higher [AT] values in domesticated accessions relative to wild accessions, or [AT]-increase, are consistently observed for SNPs found in either genic or non-genic portions of the genome, with non-genic SNPs having a greater contribution to the [AT]-increase. Interestingly, we also find that the divergence in [AT] is much higher in pericentromeric regions than in other regions. All 4 sequence motifs related to solar-UV signature consistently have higher frequencies in methylated regions than unmethylated regions. With a different set of population-private SNPs, we also discover the enrichment of mutations related to the solar-UV signature in domesticated accessions. Using base-composition across polymorphic sites as the phenotype, genome-wide scans identify a set of putative candidate genes involved in UV damage repair pathways. Together, these findings seem to suggest that solar-UV radiation and differential mutation repair are critical components in the genome divergence process that resulted in domesticated accessions’ greater numbers of nucleotides A and T.


Gene Flow and Mutation

A population’s genetic variation changes as individuals migrate into or out of a population and when mutations introduce new alleles.

Learning Objectives

Explain how gene flow and mutations can influence the allele frequencies of a population

Key Takeaways

Key Points

  • Plant populations experience gene flow by spreading their pollen long distances.
  • Animals experience gene flow when individuals leave a family group or herd to join other populations.
  • The flow of individuals in and out of a population introduces new alleles and increases genetic variation within that population.
  • Mutations are changes to an organism’s DNA that create diversity within a population by introducing new alleles.
  • Some mutations are harmful and are quickly eliminated from the population by natural selection harmful mutations prevent organisms from reaching sexual maturity and reproducing.
  • Other mutations are beneficial and can increase in a population if they help organisms reach sexual maturity and reproduce.

Key Terms

  • gene flow: the transfer of alleles or genes from one population to another
  • mutation: any heritable change of the base-pair sequence of genetic material

Gene Flow

An important evolutionary force is gene flow: the flow of alleles in and out of a population due to the migration of individuals or gametes. While some populations are fairly stable, others experience more movement and fluctuation. Many plants, for example, send their pollen by wind, insects, or birds to pollinate other populations of the same species some distance away. Even a population that may initially appear to be stable, such as a pride of lions, can receive new genetic variation as developing males leave their mothers to form new prides with genetically-unrelated females. This variable flow of individuals in and out of the group not only changes the gene structure of the population, but can also introduce new genetic variation to populations in different geological locations and habitats.

Gene flow: Gene flow can occur when an individual travels from one geographic location to another.

Maintained gene flow between two populations can also lead to a combination of the two gene pools, reducing the genetic variation between the two groups. Gene flow strongly acts against speciation, by recombining the gene pools of the groups, and thus, repairing the developing differences in genetic variation that would have led to full speciation and creation of daughter species.

For example, if a species of grass grows on both sides of a highway, pollen is likely to be transported from one side to the other and vice versa. If this pollen is able to fertilize the plant where it ends up and produce viable offspring, then the alleles in the pollen have effectively linked the population on one side of the highway with the other.

Mutation

Mutations are changes to an organism’s DNA and are an important driver of diversity in populations. Species evolve because of the accumulation of mutations that occur over time. The appearance of new mutations is the most common way to introduce novel genotypic and phenotypic variance. Some mutations are unfavorable or harmful and are quickly eliminated from the population by natural selection. Others are beneficial and will spread through the population. Whether or not a mutation is beneficial or harmful is determined by whether it helps an organism survive to sexual maturity and reproduce. Some mutations have no effect on an organism and can linger, unaffected by natural selection, in the genome while others can have a dramatic effect on a gene and the resulting phenotype.

Mutation in a garden rose: A mutation has caused this garden moss rose to produce flowers of different colors. This mutation has introduce a new allele into the population that increases genetic variation and may be passed on to the next generation.


Module 7 Lab 1 Natural Selection With Goldfish

organisms. In this lab, we will be using goldfish crackers to aid us in understanding natural selection and evolution. The population of fish has two traits from the characteristic of color. One trait will be designated as adaptive to the environment, and the other will be considered non- adaptive.

Background story: You are a piscivore, a fish that eats other fish. The species you like to eat comes in two forms: light-colored and dark-colored. You eat the fish that are easiest to find in their surroundings. Since the fish you eat swim near the top of the pond and you hunt from below, the dark-colored fish are easier to see from below and eaten more often. Since the dark colored-trait is recessive, the dark-colored fish are homozygous recessive. Because the light-colored trait is dominant, the light-colored fish are either homozygous or heterozygous dominant.

Materials: On campus, we use original, cheddar, and pretzel goldfish crackers

To represent the different types of fish. You may use any edible snack that comes

In two light colors and one dark color. (You could also make paper fish.)

This is a link to a video demonstrating how to complete this lab, including how

To do the calculations.

https://zoom.us/rec/share/- MB7Frvb1kFIW5GRuWKAfu0dD56maaa81HVPqPMPnhq0fCp2ZwqJbIv93wdaYyRi (Access Password: T1=g=5x8)

Procedure:

You will observe natural selection according to the above story. You will follow the change in the population of fish over five generations. On the Data and Observation page, predict the outcome of predation on the population over the five generations.

Create a source population of approximately equal numbers of original (homozygous dominant), cheddar (heterozygous), and pretzel (homozygous recessive) fish. Obtain a population of 32 fish randomly selected from your source population to be the first generation. Record the number of homozygous dominant fish (original), heterozygous fish (cheddar), and homozygous recessive (pretzel) fish in Table 1 on the Data and Observation sheet.

Calculate the allele frequency as if the population was in Hardy-Weinberg Equilibrium and enter the data in 3 on the Data and Observation sheet.

The general formulas for calculating Hardy-Weinberg Equilibrium are p + q = 1 and p 2 + 2pq + q 2 = 1 Where p = the frequency of the dominant (light) allele. q = the frequency of the recessive (dark) allele.

p 2 = the frequency of homozygous dominant individuals 2pq = the frequency of heterozygous individuals. q 2 = the frequency of homozygous recessive individuals.

To find the frequency of p you need to add up all the p alleles (2 from each AA fish and 1 from each Aa fish) and divide by the total number of alleles (64, two in each of the 32 fish).

Say your original population is 14 AA (original), 9 Aa (cheddar), 9 aa (pretzel).

This population has 14 + 14 + 9 A alleles. Divided by 64 total alleles. This gives p = 0.578. This population has 9 + 9 + 9 a alleles. Divided by 64 total alleles. This gives q = 0.

Eat four dark-colored fish. (If you do not have enough dark-colored fish, then randomly pick some light-colored fish to eat.) Enter the number of fish of each color after predation in Table 2 on the Data and Observation page.

Obtain a new generation. The new generation will also have 32 fish. The first step to finding the new generation is to calculate p and q after predation and enter these numbers in Table

To find the frequency of p you need to add up all the p alleles (2 from each AA fish and 1 from each Aa fish) and divide by the total number of alleles which is now 56.

Continuing the example from above, you now have 14 AA fish, 9 Aa fish, and 5 aa fish. p = (14 + 14 + 9)/56 = 0. q = (9 + 5 + 5)/56 = 0.

New generation numbers will be: AA = p 2 x 32 = 0.661 x 0.661 x 32 = 14

Aa = 2pq x 32 = 2 x 0.661 x 0.339 x 32 = 14

aa = q 2 x 16 = 0.339 x 0.339 x 32 = 4

Enter the number of each type of fish that will be in the next generation in Table 1.

Repeat steps 3 and 4 three more times.

Calculate the allele frequencies of generation 5 and enter them in 5 on the Data and Observation Sheet.

On the Data and Observation page, write a paragraph describing what happened to each type of fish and explain why. Contrast the conclusions derived with your original predictions.

Answer the remaining questions.

Add a picture of your fish in their pond and a selfie of you being a predator.

What happened to each color of fish and why? Did your original predictions agree with the outcome? If not, how did they differ? The original and cheddar stayed the same population while the red fish decreased in population due to predation.

Which trait is not favorable? Why? Aa its recessive and was primarily attacked through predation compared to the other fish.

Which phenotype is reduced in the population? aa homozygous recessive

Did this phenotype disappear from the population? Why or why not? Not completely but seems it would over time.

Explain why the recessive allele (a) does not disappear from the population. because there will always be an offspring as the genes evolve. After there are no more recessive genes the AA and Aa will produce an offspring of a

Did evolution occur? Explain. Yes the evolution processes is quick which leads to evolution.

Explain what would happen if the selection pressure changed and the dark-colored fish were less likely to be eaten. Then the aa recessive gene would have been more prominent

What would happen if it were better to be heterozygous (Aa)? Will there be homozygous fish? Explain. Yes because there would then be a 50/50 chance of the recessive gene


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