Protein Synthesis Lab Analysis

There are two main steps to make a protein: transcription and translation. In transcription, a section of DNA is copied, producing messenger RNA. In translation, the RNA reaches a ribosome. The ribosome reads bases 3 at a time. Each 3-base sequence corresponds to an amino acid, which the ribosome adds to the protein it is creating. After that, the amino acid chain folds and becomes a protein.



There were three different types of mutations we tested: substitution, insertion, and deletion. Substitution either caused a great change or a very small change. Sometimes, it caused no change at all. Substitution was only an effective mutation when it was placed in a strategic position. Insertion and deletion both caused major changes when done at the beginning of a sequence. However, towards the end of a sequence, insertion and deletion caused much smaller changes.



During this lab, I was allowed to choose a mutation of my own to test. I chose to test substitution, because after looking at the bases of the gene I was given, I realized I could easily substitute strategic nucleotides in order to get a drastically different result. I substituted two nucleotides in the beginning of the sequence, turning TAC into ATC. This changed the resulting RNA sequence from AUG to UAG. Basically, I changed the start codon to the stop codon. As you can imagine, the amino acids of the resulting protein were very much changed. Instead of the protein Met-Tyr-Lys-His-Val-Ile-Asn-Cys-Ile, there was no protein at all. This mutation changed more amino acids than any other tested. Obviously, placement did matter; if I just substituted bases at random, I would not have gotten the same result.



Mutations could affect our lives in many ways. An example of a mutation is Huntington disease. According to the U.S. National Library of Medicine's Genetic Home Reference, Huntington disease is caused by a mutation in the HTT gene, which provides instructions to make the huntingtin protein. Usually, in this gene, the sequence of cytosine, adenine, and guanine is repeated 10 to 35 times. However, within those with Huntington disease, this sequence is repeated much more, making the mutation an insertion. The length of the sequence of cytosine, adenine, and guanine creates very long huntingtin proteins, which are cut apart and bind together. This eventually causes neurons to die. Huntington disease is inherited with an autosomal dominant pattern.