Prader-Willi syndrome (PWS) is a gentic disorder which has an impact on numerous physiological systems. PWS affected individuals (specifically babies) experience delayed growth, significant hypotonia (low muscle tone), and feeding issues. It does effect circadian rhythms in mice models.
SNORD116, often referred to as HBII-85, is a non-coding RNA (ncRNA) molecule that contributes to the alteration of other small nuclear RNAs (snRNAs). Unlike the majority of other snoRNAs, SNORD116 is not significantly complementary to ribosomal RNA and is expressed widely in the brain (but not in PWS patients).
According to the studies, SNORD116 cause sleep defect in patients with Prader-Willi syndrome. Same observation was seen in mouse models too. Paternal expression of SNORD116 is thought to be a potential gene for the sleep disruptions/circadian rhythm’s that the majority of PWS sufferers.
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A mistake in DNA replication before meiosis produces an organism that is better able to outrun predators.
Explanation:
The genetic variation results from the different alleles of a population. The mutation or mistake in DNA replication would cause gene variants which may be beneficial. The variation in the DNA sequence of genome results in variants in small population.
Genetic variation is the cause of natural selection and eventually, evolution takes place with beneficial traits.
It is mentioned in the question that resulting offspring having received the mutant allele could result in better surviving capabilities or phenotypic traits as they are able to outrun predators.
The answer to that is, Chlorine
