Prader-Willi and Angelman syndromes are human conditions that result in part through the process of genomic imprinting, where a particular gene is “marked” during gamete formation in the parent of origin. In the case of these two syndromes, a portion of the long arm of chromosome 15 (15q11 to 15q13) is imprinted. Another condition, Beckwith-Wiedemann syndrome (accelerated growth and increased risk of cancer), is associated with abnormalities of imprinted genes on the short arm of chromosome 11. All three of the above syndromes occur when imprinted sequences become abnormally exposed by some genetic or chromosomal event. One such event is uniparental disomy (UPD), in which a person receives two homologs of one chromosome (or part of a chromosome) from one parent and no homolog from the other. In many cases, UPD is without consequence; however, if chromosome 11 or 15 is involved, then, coupled with genomic imprinting, complications can arise. Listed below are possible origins of UPD. Provide a diagram and explanation for each.
1. Trisomic rescue: loss of a chromosome in a trisomic zygote
2. Monosomic rescue: gain of a chromosome in a monosomic zygote
3. Gamete complementation: fertilization of a gamete with two copies of a chromosome by a gamete with no copies of that chromosome
4. Isochromosome formation: a chromosome that contains two copies of an arm (15q-15q, for example) rather than one.
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