Recombinant human insulin (made by inserting human DNA encoding insulin into E. coli) is one of the most widely used recombinant pharmaceutical products in the world. What segments of the human insulin gene are used to create recombinant bacteria that produce human insulin?
Table of contents
- 1. Introduction to Genetics51m
- 2. Mendel's Laws of Inheritance3h 37m
- 3. Extensions to Mendelian Inheritance2h 41m
- 4. Genetic Mapping and Linkage2h 28m
- 5. Genetics of Bacteria and Viruses1h 21m
- 6. Chromosomal Variation1h 48m
- 7. DNA and Chromosome Structure56m
- 8. DNA Replication1h 10m
- 9. Mitosis and Meiosis1h 34m
- 10. Transcription1h 0m
- 11. Translation58m
- 12. Gene Regulation in Prokaryotes1h 19m
- 13. Gene Regulation in Eukaryotes44m
- 14. Genetic Control of Development44m
- 15. Genomes and Genomics1h 50m
- 16. Transposable Elements47m
- 17. Mutation, Repair, and Recombination1h 6m
- 18. Molecular Genetic Tools19m
- 19. Cancer Genetics29m
- 20. Quantitative Genetics1h 26m
- 21. Population Genetics50m
- 22. Evolutionary Genetics29m
11. Translation
The Genetic Code
Problem 29b
Textbook Question
Shown here are the amino acid sequences of the wild-type and three mutant forms of a short protein.
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Wild-type: Met-Trp-Tyr-Arg-Gly-Ser-Pro-Thr
Mutant 1: Met-Trp
Mutant 2: Met-Trp-His-Arg-Gly-Ser-Pro-Thr
Mutant 3: Met-Cys-Ile-Val-Val-Val-Gln-Hi
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Use this information to answer the following questions:
For each mutant protein, determine the specific ribonucleotide change that led to its synthesis.

1
Step 1: Understand the wild-type amino acid sequence and the corresponding codons. Recall that each amino acid is encoded by a set of three ribonucleotides (a codon) in the mRNA, which is transcribed from the DNA sequence.
Step 2: Compare the mutant amino acid sequences to the wild-type sequence to identify where changes occur. For Mutant 1, note that the sequence is truncated after the second amino acid; for Mutant 2, observe the substitution of 'His' for 'Tyr' at the third position; for Mutant 3, note the completely different sequence starting from the second amino acid.
Step 3: For each mutant, determine the type of mutation that could cause the observed change: a nonsense mutation (introducing a stop codon) for truncation, a missense mutation (single amino acid substitution), or a frameshift mutation (altering the reading frame and thus the entire downstream sequence).
Step 4: Use the genetic code table to identify the specific codons for the wild-type and mutant amino acids at the positions where changes occur. Then, deduce the single ribonucleotide change(s) in the mRNA codon that would convert the wild-type codon into the mutant codon.
Step 5: Translate the mRNA codon changes back to the DNA sequence changes by replacing uracil (U) with thymine (T), thus identifying the specific ribonucleotide (or nucleotide) substitution, insertion, or deletion in the DNA that led to the mutant protein synthesis.

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Key Concepts
Here are the essential concepts you must grasp in order to answer the question correctly.
Genetic Code and Codon-Amino Acid Relationship
The genetic code consists of nucleotide triplets called codons, each specifying a particular amino acid. Understanding how codons translate into amino acids is essential to link changes in nucleotide sequences to alterations in protein sequences. This relationship allows prediction of nucleotide mutations based on observed amino acid substitutions.
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The Genetic Code
Types of Mutations and Their Effects on Protein Sequence
Mutations such as nonsense, missense, and frameshift mutations alter the nucleotide sequence, impacting the resulting protein. Nonsense mutations introduce premature stop codons, truncating proteins; missense mutations change one amino acid; frameshifts alter the reading frame, drastically changing downstream amino acids. Recognizing these helps infer nucleotide changes from protein differences.
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Point Mutations
Translation Termination and Its Impact on Protein Length
Translation stops when a stop codon (UAA, UAG, UGA) is encountered, resulting in protein termination. Mutations that create premature stop codons produce shorter proteins, as seen in truncated mutants. Understanding stop codons and their role in ending translation is crucial to explain why some mutant proteins are shorter than the wild-type.
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Translation Termination
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