Genetics Original Gene Sequence: 3\'-T AC CC

Genetics

Original Gene Sequence: 3'-T AC CC T. TT AGTAGCCAC T-5

Transcription of Original: 3'-A UG GG A AA UCAUCGGUG A-5'

Translation of Original: Start codon Met, Gly, Asn, His, Arg, Stop

Mutated Gene Sequence 1: 3'-T ACGCT TT AGTAGCCAT T-5'

Transcription of Mutated 1: 3'-A UGCGA AA UCAUCGGUA A-5'

Translation of Mutated 1: Start codon Met, Arg, Asn, His, Arg, Stop

Mutated Gene Sequence 2: 3'-T AACCT TT ACTAGGCAC T-5'

Transcription of Mutated 2: 3'-AUUGGAAAUGAUCCGUGA

Translation of Mutated 2: Ile, Gly, Asn, Asp, Pro, Stop

The first and last codons of the sequences are the start and stop codons respectively. The start codon indicates where transcription should begin. The stop codon indicates where transcription should end.

When a mutation occurs in the start codon, transcription will not be initiated and thus a protein will not be produced. When a mutation in the stop codon occurs sometimes the mutation will still encode for a stop codon as was the case with mutated gene sequence 1 above. However, if the mutation does not code for a stop codon then transcription will continue causing the transcript to be incorrect for a particular protein and the resulting amino acid sequence will not produce a functional protein.

3. Mutated gene sequence 1 does encode for a different protein than the original gene sequence. Amino acid glycine in the original sequence is replaced by arginine in the mutated gene sequence. Since mutated gene sequence 2 does not include a start codon transcription will not be initiated therefore no protein will be produced.

4. The amino acid sequence is important because it allows the protein to fold a particular way. A functional protein must have the proper structure. For example, a mutation that replaces a cysteine with another amino acid may knock out a critical cysteine bond in the folding of the protein so that it will not have a functional structure.

Part II:

1. Cystic Fibrosis:

C

c

C

CC

Cc

c

Cc

cc

2. There is a 25% chance that the child will be healthy and not a carrier of the cystic fibrosis trait indicated by the CC alleles. There is a 50% chance that the child will be healthy and a carrier of the cystic fibrosis trait indicated by the Cc alleles. There is a 25% chance that the child will have cystic fibrosis indicated by the cc alleles.

Part III:

Sexual reproduction is an important source of genetic variation. As opposed to the process of asexual reproduction that produces exact copies of the parent cell. Three mechanisms that create genetic variation in sexual reproduction are random fertilization, random assortment of chromosomes during gamete production, and crossing over of non-homologous sister chromatids during meiosis.

In sexual reproduction each parent donates genetic material that makes up the genetic material of the offspring (Bailey, 2011). This occurs with special cells called gametes that are produced by a type of cell division called meiosis. Meiosis differs from simple mitosis or cell division. Meiosis is a two part cell division that creates four daughter cells with only one set of chromosomes each. In the process of meiosis the chromosomes of the parent are randomly assorted in the gametes creating genetic variation (Schorderet-Slatkine, 2008). Also during prophase I of meiosis crossing over of non-homologous sister chromatids occurs thus creating even more genetic variation (Campbell, 2008). Crossing over occurs when two chromosomes are aligned close together causing strain and breakage, which is repaired by the cell but can put pieces of one chromosome back on the other sister chromatid instead of in its original position.