What genetic alteration is associated with Prader-Willi Syndrome?

Prader-Willi Syndrome is primarily associated with the absence of genetic material on the paternal copy of chromosome 15. It typically arises due to a deletion in the 15q11-q13 region on the paternal chromosome, which leads to the characteristic symptoms of the syndrome, such as hyperphagia, obesity, and developmental delays.

In this context, the lack of genetic material on chromosome 15 directly impacts the functions of genes that are normally expressed from the paternal allele. Since the maternal copy of this region is imprinted and silenced, the absence of the paternal genes results in the clinical features observed in individuals with Prader-Willi Syndrome.

The other options do not accurately describe the genetic basis of the syndrome. A duplication of chromosome 15 does not align with the genetic mechanism of Prader-Willi Syndrome, and translocation with chromosome 21, as well as mutations in the coding region of chromosome 7, are unrelated to the etiology of this condition. Understanding these facets of Prader-Willi Syndrome helps in recognizing the genetic underpinnings of the disorder.