43) You are studying mutations in a bacterical gene that codes for an enzyme who

Question

43) You are studying mutations in a bacterical gene that codes for an enzyme whose amino acid seqence is known. In the wild-type protein, proline is the fifth amino acid from the amino terminal end. In one of your mutants with nonfunctional enzyme, you find a serine at position number 5. You subject this mutant to further mutagenesis and recover three different strains. Strain A has a proline at position number 5 and acts just like wild type. Strain B has trypophan at position number 5 and also acts like wild type. Strain C has no detectable enzyme function at any temperature, and you can't recover any protein that resembles the enzyme. You mutagenize strain C and recover a strain (C-1) that has enzyme function. The second mutation in C-1 responsible for the recovery of enzyme function does not map at the enzyme locus.

a)                    Sequence (You need three bases on each strand.)

            Put in the box to the right.   

        b)    Be brief.

        c)    Mutation____________

        d)    Second mutation___________

Explanation / Answer

Answer:

a) The sequence of nucleotides on the RNA-like strand of the wild-type and mutant genes at this position must be:

wild type   5? G G T/C 3?
mutant 1   5? T G T/C 3?
mutant 2   5? G T T/C 3?
mutant 3   5? A G T/C 3?
mutant 4   5? G A T/C 3?
mutant 5   5? C G T/C 3?
mutant 6   5? G C T/C 3?   

b) An example of a portion of the T4 rIIB gene in which Crick and Brenner had recombined one + and one ? mutation is shown here. (The RNA-like strand of the DNA is shown.)

wild type   5? AAA AGT CCA TCA CTT AAT GCC 3?
mutant   5? AAA GTC CAT CAC TTA ATG GCC 3?

c) An understanding of the principles of translation and RNA splicing are needed to answer this question. Because there is an extension on the C-terminal end of the protein, the mutation probably affected the termination (nonsense) codon rather than affecting splicing of the RNA. This could have been a base change or a frameshift or a deletion that altered or removed the termination codon. The information in the mRNA beyond the normal stop codon would be translated until another stop codon in the mRNA was reached. A splicing defect could explain Hb Constant Spring only in the more unlikely case that an incorrectly spliced mRNA would encode a protein much longer than normal.

d) Second mutation is promoter mutation.

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