One bad copy is the whole story
In an autosomal dominant disorder, a single faulty copy is enough to cause disease, even though a perfectly good copy sits right beside it. The disease allele is a dominant allele — written D — so genotypes Dd and DD are both affected, and only dd is unaffected. Huntington disease and achondroplasia are textbook examples.
Why doesn't the good copy save the day, as it does in recessive disease? Usually because the fault is not a simple loss of function. In a gain-of-function mutation, the altered protein actively does harm — in Huntington disease, a misfolded protein accumulates and poisons neurons, and no amount of normal protein can mop it up. In a dominant-negative effect, the bad protein jams the machinery the good copies are trying to build. Either way, having one good copy is not enough.
The 50% rule
Because an affected person is usually heterozygous (Dd), each child has a one-in-two chance of inheriting the disease allele. The cross is Dd x dd, and the Punnett square is strikingly simple.
Cross: Dd x dd (affected parent x unaffected parent)
affected parent
| D | d
----+-----+-----
un d | Dd | dd
aff | |
----+-----+-----
par d | Dd | dd
ent | |
Children: 1/2 Dd (AFFECTED) : 1/2 dd (unaffected)
=> 50% of children inherit the disorder, each pregnancy.
The trait appears in EVERY generation (vertical pedigree).
Unaffected children (dd) cannot pass it on.Not everyone shows it the same way
Dominant does not mean rigidly predictable. Penetrance asks: of everyone carrying the allele, what fraction actually show any sign of the disease? When penetrance is below 100%, a carrier can stay symptom-free yet still pass the allele on — so a disorder can appear to “skip” a generation. Expressivity asks a different question: among those who are affected, how strongly? Some show mild signs, others severe. These two ideas explain much of the variability families notice.