Questions: Dominance, Recessiveness, and Allelic Interactions

Question 1

A pea plant shows tall stem height (the dominant phenotype). You want to determine whether it is TT or Tt. Which cross would conclusively reveal heterozygosity, and what result would confirm it?

• A. Cross with another tall plant; if any short offspring appear, the original was heterozygous
• B. Cross with a homozygous recessive (tt) plant; if any short offspring appear, the original was heterozygous (Tt)
• C. Cross with a homozygous recessive (tt) plant; if all offspring are tall, the original is definitively TT
• D. Self-fertilize; a 3:1 ratio proves the original was Tt

Answer: (B)

The test cross — mating an unknown genotype with the homozygous recessive (tt) — is the definitive tool. A Tt × tt cross yields 50% Tt (tall) and 50% tt (short); any short offspring prove the unknown parent contributed a t allele, confirming Tt. Option 2 is incomplete: all-tall offspring from a test cross make TT probable but not certain with small samples (by chance, a Tt × tt cross could produce all tall offspring). Option 0 is insufficient because crossing two tall plants (both possibly Tt) might yield 0 short offspring by chance.

Question 2

A geneticist discovers a new dominant disorder and says: 'This allele must be common in the population since dominant alleles always spread quickly.' Why is this reasoning flawed?

• A. Dominant alleles cannot cause disease — only recessive alleles cause genetic disorders
• B. Allele frequency is determined by selection, genetic drift, and mutation rate — not by dominance. Many dominant alleles are rare; many recessive alleles are common
• C. The disorder being dominant means heterozygotes are always affected, which would rapidly eliminate the allele
• D. Dominant alleles only spread quickly in small populations, not large ones

Answer: (B)

Dominance and population frequency are completely independent. Huntington's disease is caused by a dominant allele yet is rare because it reduces fitness after reproductive age. The sickle cell allele is recessive yet common in malaria-endemic regions because heterozygous carriers have a survival advantage. Allele frequency is governed by natural selection, genetic drift, mutation pressure, and gene flow — none of which depend on whether the allele is dominant or recessive.

Question 3

A dominant allele is stronger, more functional, or biologically superior to its recessive counterpart.

• T. True
• F. False

Answer: False

Dominance is purely a description of what phenotype appears in a heterozygote — it carries no implication of superiority or functionality. Huntington's disease is caused by a dominant gain-of-function mutation that is severely harmful. Many recessive alleles encode fully functional proteins. 'Dominant' and 'recessive' are relational labels describing expression patterns in heterozygotes, not rankings of quality or biological value.

Question 4

Two individuals with identical phenotypes can have different genotypes, and a test cross is required to reveal this hidden genetic difference.

• T. True
• F. False

Answer: True

Under complete dominance, both AA and Aa individuals express the dominant phenotype and are phenotypically indistinguishable. Their genotypes differ, but the recessive allele in the heterozygote is masked. A test cross with a homozygous recessive (aa) reveals the difference: Aa × aa produces 50% recessive-phenotype offspring, while AA × aa produces none. This is the foundational logic of Mendelian genetic analysis — phenotype alone cannot distinguish AA from Aa.

Question 5

Why are most newly arising loss-of-function mutations recessive, and what molecular mechanism underlies this pattern?

Model answer: Most genes encode enzymes or structural proteins, and for many, a single functional copy produces enough product to carry out the normal biological function (haplosufficiency). A loss-of-function mutation breaks one copy, but the second working copy compensates. In a heterozygote, half the normal protein amount is still sufficient, so the mutant allele is invisible phenotypically — it is recessive. Only when both copies are non-functional (homozygous recessive) does the phenotype appear.

This molecular logic also explains when dominant mutations arise: either as gain-of-function (the mutant protein does something harmful the normal protein doesn't) or as haploinsufficiency (the gene is so dosage-sensitive that one copy is not enough for normal function). These are less common mechanisms, which is why most newly arising mutations are recessive and why genetic disease often requires inheriting two defective copies.