Revision summary
Imprinting silences one parental copy of a gene. Haig tied the logic to parental conflict over growth. Paternal versus maternal loss at 15q yields Prader–Willi or Angelman. Beckwith–Wiedemann and Silver–Russell are growth-side examples. Counselling must record which parent transmitted the region.
Model answer
Introduction
Imprinting is parent-of-origin silencing of a gene. The same deletion can therefore cause two different diseases according to whether the chromosome came from the mother or the father.
Body
The mechanism
- Epigenetic marks, not a change of DNA letters, switch one parental copy off. David Haig linked this to parental conflict over foetal growth.
- Chromosome 15q is the teaching human region.
Disease pairs
- Prader–Willi syndrome follows loss of the paternal 15q contribution. Angelman syndrome follows loss of the maternal UBE3A copy.
- Beckwith–Wiedemann and Silver–Russell growth disorders involve imprinted loci on 11p.
- Hydatidiform moles and some cancers show imprinting errors. Pedigree counselling must ask which parent transmitted the chromosome.
Anthropological note
- This is non-Mendelian at the phenotype even though the deletion can be mapped. A simple dominant chart fails.
Flow diagram
flowchart TD I[Imprint] --> F[Father copy on] I --> M[Mother copy on] F --> PW[Prader Willi] M --> AN[Angelman]
Conclusion
Imprinting makes parent of origin a clinical fact. Prader–Willi and Angelman are the pair every counsellor names.
Quick related
Students also ask
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Discuss how anthropological knowledge of the human body may be used in designing equipments and articles of human use
Next question on this syllabus topic (2022 · Q8(c)). View answer →
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Can a pedigree look Mendelian and still be imprinted?
Transmission may look dominant, but only one parental origin produces the disease. That is the clue.
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Is imprinting the same as sex linkage?
No. Sex linkage is on X or Y. Imprinting can sit on an autosome and still care which parent it came from.
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