Variation comes before selection. More genotypes means better odds that someone survives the next disease.
When a new disease or pesticide arrives, the survivors tend to be the ones already carrying helpful alleles. A diverse population probably has some. A clonal or small inbred population may have none.
Key terms
- Genetic variation — differences in alleles among the individuals of a population. It is the raw material natural selection works on.
- Mutation — a change in DNA sequence. In cells that make eggs or sperm, it is the only source of brand-new alleles.
- Recombination — the reshuffling done by sexual reproduction: crossing over, independent assortment, and random fertilization. New combinations, no new alleles.
- Heterozygosity — the share of genes where an individual carries two different alleles. Averaged over a population, it measures genetic diversity.
- Clone — a genetically identical copy, like a tree grown from a cutting. A field of clones is effectively one genotype.
- Inbreeding — mating between relatives. Offspring are homozygous at more genes, so harmful recessive alleles are expressed more often.
How it works
- Mutation adds new alleles, rarely and at random. A new threat does not trigger the mutations that would help against it.
- Sexual reproduction reshuffles those alleles every generation, so almost every offspring carries a combination no one has carried before.
- A new pressure arrives: a pathogen, a pesticide, a drought. Individuals whose alleles happen to suit it survive and reproduce more, so those alleles become more common.
- An allele's value depends on the environment. The sickle-cell allele protects carriers against malaria. Where malaria is absent, it offers no benefit and still causes disease in homozygotes.
- Low variation can mean no survivors. Clones, crop monocultures, and small inbred populations can be wiped out by a single pathogen strain.
- Small populations lose variation faster. Genetic drift drops alleles by chance, and inbreeding raises homozygosity. Gene flow from another population can restore diversity.
Why it matters
Expect two populations facing the same threat: one sexual and one clonal, or one large and one small. Pick the one with more genotypes as the likelier to have survivors. When a table gives both size and heterozygosity, find the population where they disagree. That case shows which one survival tracks.
Exam traps
| Trap | Actually |
|---|
| The pesticide made the insects resistant, and the survivors passed that on. | A few insects already carried resistance alleles. The spray killed most others, so those carriers founded the next generation. |
| Crossing over and independent assortment create new alleles. | They reshuffle alleles that already exist. Only mutation makes a new allele. |
| A clonal crop resists disease well, since every plant shares any resistance. | Every plant also shares every weakness. One pathogen strain that beats that genotype can kill the whole stand. |
| The bigger population is always the healthier one. | Check genetic diversity, not only head count. A small population that keeps its alleles can do well. |
Worked example
An isolated population of 30 wild cats has low genetic diversity, and many kittens are born with heart defects. Researchers release 8 unrelated females from a distant population of the same species. Before the release: 30 adults, mean heterozygosity 0.18, heart defects in 22% of kittens, kitten survival to age 1 of 35%. Five years later: 41 adults, heterozygosity 0.31, defects 7%, survival 61%. Ten years later: 85 adults, heterozygosity 0.33, defects 5%, survival 64%. What best explains the jump in kitten survival during the first five years?
- Find what changed first. In five years, heterozygosity rose from 0.18 to 0.31 and defects fell from 22% to 7%, but the adult count grew only from 30 to 41.
- Name the source. The released females brought alleles the isolated cats had lost, so their kittens were heterozygous at many more genes.
- Link diversity to survival. In an inbred population, harmful recessive alleles are often homozygous and expressed. Paired with a working allele, they are masked.
- Test the size explanation. From year 5 to year 10 the population doubled, yet survival barely moved. Size did not drive the jump.
Gene flow from the released females raised heterozygosity, so fewer kittens were homozygous for harmful recessive alleles. Fewer kittens had defects, and more survived.
Survival rose with heterozygosity, then stayed nearly flat while the head count doubled. So diversity, not size, explains the jump. The near-miss is 'the population got bigger.' Most of that growth came after survival improved, so it looks like a result, not a cause.