Reference no: EM132405326

Double-muscling from myostatin mutations and callipyge mutations share some similarities in terms of phenotype.

1) Describe the double-muscling and callipyge mutation phenotypes of livestock including their advantages and disadvantages.

2) How is the cell cycle affected by each mutation? How is protein synthesis and degradation affected by each mutation? Does this alter the effectiveness of the mutations in terms of prenatal vs postnatal development?

3) What would the phenotype be of an animal that possessed two mutated copies of myostatin (rendering myostatin non-functional) and a mutated copy of the callipyge locus from the paternal side (normal from maternal side)? Why would this be?