AP Biology · Unit 7 · Topic 7.11
Variations in Populations
Two populations can contain the same number of organisms and still differ sharply in their capacity to respond to a new drought, pathogen, or temperature regime. The difference may lie not in population size but in which heritable variants are present and how common they are. Genetic diversity supplies possible responses; the environment determines which of those possibilities matter.
Variation is the raw material, not a promise
Genetic variation consists of inherited DNA differences among individuals, including different alleles at a locus and different combinations of alleles across loci. Phenotypic variation is the observable variation in traits. Phenotypes can reflect genotype, environment, and interactions between them, so visible differences do not automatically demonstrate genetic differences.
Mutation can create a new allele. Crossing over, independent assortment, and random fertilization reorganize existing alleles into new combinations, while gene flow can carry alleles from another population. These processes do not create only beneficial variation. A new or imported allele may be advantageous, neutral, or harmful under the conditions in which its carriers live.
Natural selection can change a population through heritable differences in reproductive success. If every plant grows shorter during a dry week because its cells lose water, that response is phenotypic variation, but it does not by itself establish inherited variation or evolution. A useful explanation must connect genotype to phenotype, phenotype to reproductive contribution, and reproductive contribution to a change across generations.
Diversity has more than one dimension
Simply counting the number of alleles gives allelic richness. The frequencies of those alleles add another dimension: two populations may each contain alleles \(A_1\) and \(A_2\), yet one may be nearly fixed for \(A_1\) while the other contains both at similar frequencies.
One quantitative extension is expected heterozygosity. If the allele frequencies at a locus are \(p_1,p_2,\ldots,p_k\), then
The sum is the probability that two independently sampled allele copies have the same allelic identity under the sampling model; subtracting from 1 gives the probability that they differ. For two alleles with frequencies \(p\) and \(q\), where \(p+q=1\), this becomes
| Population | \(p(A_1)\) | \(q(A_2)\) | Allelic richness | \(H_E=2pq\) |
|---|---|---|---|---|
| A | 0.50 | 0.50 | 2 | \(2(0.50)(0.50)=0.50\) |
| B | 0.90 | 0.10 | 2 | \(2(0.90)(0.10)=0.18\) |
Both populations have two alleles, but a randomly paired set of allele copies is more likely to differ in Population A. \(H_E\) is a model-based probability, not automatically the observed percentage of heterozygous organisms. Population structure, nonrandom mating, selection, and sampling error can make observed heterozygosity differ from the expectation.
Use genotype frequencies to predict a response
Consider two invented diploid plant populations, each containing 100 adults before a drought. At one locus, Population L has 90 \(A_1A_1\), 10 \(A_1A_2\), and no \(A_2A_2\) individuals. Population H has 25, 50, and 25, respectively. Under a no-drought control, each genotype has an assumed survival probability of 0.80. During drought, the assumed probabilities are 0.20 for \(A_1A_1\), 0.45 for \(A_1A_2\), and 0.75 for \(A_2A_2\).
| Population | Starting genotypes | No-drought expectation | Drought expectation |
|---|---|---|---|
| L: low \(A_2\) frequency | 90, 10, 0 | \(100(0.80)=80\) | \(90(0.20)+10(0.45)=22.5\) |
| H: balanced frequencies | 25, 50, 25 | \(100(0.80)=80\) | \(25(0.20)+50(0.45)+25(0.75)=46.25\) |
The chart does not show that “more diversity always wins.” Population H has more \(A_2A_2\) individuals, and \(A_2A_2\) was assigned the highest survival under this particular drought. A different environment that favors \(A_1\) could reverse the result. Nor does survival alone establish long-term adaptation: survivors must reproduce, and the relevant trait must be heritable.
Follow the allele copies after selection
In Population H, the expected drought survivors are 5 \(A_1A_1\), 22.5 \(A_1A_2\), and 18.75 \(A_2A_2\). Before calculating a frequency, check the denominator: 46.25 diploid survivors carry \(2(46.25)=92.5\) allele copies in total.
The number of \(A_2\) copies is one from each heterozygote plus two from each \(A_2A_2\) survivor:
Therefore, the post-survival \(A_2\) frequency is
The starting frequency was \(q=(50+2\cdot25)/200=0.50\). Differential survival raised the frequency among survivors in this model. That is evidence of selection at the survival stage, not a guarantee that the next generation will have exactly \(q=0.649\). Mating, fertility, migration, mutation, and random sampling can change what is transmitted.
A bottleneck can outlast the demographic crash
A population bottleneck is a sharp reduction in the number of breeding individuals. The survivors carry only a sample of the original gene pool, so rare alleles can disappear by chance even when they were neither harmful nor helpful. A founder event applies the same sampling logic when a few individuals establish a new population.
Census size and genetic diversity can recover on different schedules. Descendants of a small survivor group may multiply until the habitat again holds thousands of individuals, yet every descendant still traces its alleles to that narrow sample. Mutation can eventually create new variants and gene flow can introduce them, but numerical recovery alone does not recreate lost alleles.
The relevant genetic scale is often effective population size, \(N_e\), the size of an idealized population experiencing the same amount of drift as the real one. Unequal sex ratios, large differences in reproductive success, and fluctuating population sizes can make \(N_e\) much smaller than the head count. Thus, “many organisms are alive” does not necessarily mean that many independent allele copies reach the next generation.
Do not merge inbreeding and drift into one mechanism
Inbreeding increases mating between relatives. Under a simple model, it raises homozygosity and lowers heterozygosity but does not, by itself, require allele frequencies to change. It can bring two copies of a deleterious recessive allele together, increasing expression of harmful phenotypes and contributing to inbreeding depression.
Genetic drift, by contrast, is random change in allele frequencies caused by finite sampling. Drift is stronger in small populations and can eliminate or fix alleles. Small populations often experience both processes, which is why their effects are easy to confuse, but the causal claims differ: inbreeding concerns how alleles are paired within individuals; drift concerns which allele copies are passed on.
Allelic richness and heterozygosity can also respond differently to a bottleneck. Rare alleles may be lost quickly, reducing richness, while common alleles still maintain some heterozygosity. A single diversity statistic therefore cannot describe every potentially important form of variation.
Environmental pressure gives an allele its context
An allele does not carry a permanent label reading “adaptive.” Its fitness effect depends on the environment, genetic background, and tradeoffs among traits. An allele that improves water retention during drought might slow growth when water is abundant. A variant that resists one pathogen may carry an energetic cost when that pathogen is absent.
This context explains why genetic diversity can increase a population's chance of containing individuals that tolerate a new pressure without guaranteeing resilience. If none of the existing variants help, if the pressure is too severe, if tolerant individuals cannot reproduce, or if habitat loss removes essential resources, diversity alone will not prevent decline. Conversely, a low-diversity population can persist in stable conditions; low diversity is a risk factor, not a diagnosis of immediate extinction.
The perspective also depends on whose population is being considered. High genetic variation in a pathogen population can accelerate the appearance or spread of drug resistance, which benefits the pathogen population but harms the host. “Beneficial” must always be attached to an organism and an environment.
Design evidence that separates genes from environment
Suppose seedlings from Population L and Population H differ in drought survival in the field. That observation is not enough to assign the difference to genetic diversity, because soil, age, density, prior exposure, and maternal environment may also differ.
A stronger hypothetical experiment would sample many families from each population, grow offspring under shared conditions, randomly assign replicated groups to control and drought treatments, keep density and measurement time consistent, and measure both survival and reproductive output. Sequencing or genotyping can estimate allelic richness, allele frequencies, and heterozygosity. Replicate populations are essential because drift and sampling error can make one group unusual.
A common environment reduces some environmental differences but does not prove that one measured locus caused the response. Crosses, genotype–phenotype associations, and functional tests can strengthen that claim. Evidence should also be collected across more than one environment, because a response that looks favorable under drought may be neutral or costly elsewhere.
Gene flow can restore variation—and alter local combinations
Immigrants or their gametes can introduce alleles that were absent from an isolated population. This may increase diversity and reduce the chance that close relatives mate. In some conservation settings, carefully managed gene flow is called genetic rescue when it improves population fitness.
The outcome is not automatically positive. Incoming alleles may dilute locally adapted combinations or produce poorly matched interactions among genes and environment. The scientifically defensible question is therefore not “Is gene flow good?” but “How much gene flow, between which populations, under which ecological conditions, and with what measured consequences?”
Check the causal reasoning
1. Populations A and B each contain two alleles. Why are their \(H_E\) values 0.50 and 0.18?
Allelic richness counts two alleles in each population, but expected heterozygosity also reflects frequency. For A, \(2pq=2(0.50)(0.50)=0.50\). For B, \(2pq=2(0.90)(0.10)=0.18\). The rare \(A_2\) allele in B makes two sampled copies less likely to differ.
2. Recalculate the expected drought survivors in Population L and Population H.
For L, \(90(0.20)+10(0.45)+0(0.75)=18+4.5=22.5\). For H, \(25(0.20)+50(0.45)+25(0.75)=5+22.5+18.75=46.25\). These are expectations from assumed probabilities, not observed whole-organism counts.
3. Why does \(A_2\) rise from 0.50 to about 0.649 among Population H survivors?
The survival probabilities differ by genotype. Expected survivors contain \(22.5+2(18.75)=60\) copies of \(A_2\) among \(2(46.25)=92.5\) total allele copies, so \(q'=60/92.5\approx0.649\). More \(A_2\)-bearing genotypes survived under the invented drought conditions.
4. A bottlenecked population returns from 40 to 4,000 individuals. Has its original genetic diversity necessarily returned?
No. The 4,000 descendants may carry only alleles present in the 40 survivors. Population growth duplicates that sampled gene pool; it does not reconstruct alleles lost during the bottleneck. Mutation and gene flow may add variation later.
5. Does inbreeding necessarily change allele frequencies in one generation?
No. In the simple expectation, inbreeding changes how alleles are paired, increasing homozygotes and decreasing heterozygotes while leaving allele frequencies unchanged. Drift, selection, migration, or other processes can change the frequencies at the same time.
6. A common-garden study finds leaf-size differences between populations. Does that prove one DNA variant causes drought tolerance?
No. Shared conditions support a heritable contribution more strongly than an uncontrolled field comparison, but parental effects, many genes, and linked variables may remain. Demonstrating a specific causal variant requires genotype data and further association or functional tests, ideally across replicated environments.
Further reading: OpenStax Biology 2e — Population Genetics; Nature Scitable — Genetic Variation in a Population; U.S. Geological Survey — Genetic Diversity and Climate-Driven Range Shifts. Scope reference: College Board AP Biology Course and Exam Description, Topic 7.11. Explanations, populations, genotype counts, survival probabilities, calculations, questions, table, and SVG chart were independently written for this lesson; source figures and activities are not reproduced.
Official curriculum reference: College Board AP Biology course page. The explanation and worked example are independently written for this study site.