SOLVED PROBLEM 1. In Chapter 9, we learned that UAG and UAA codons are two of the chain-terminating nonsense triplets. On the basis of the specificity of aflatoxin B1 and ethylmethanesulfonate (EMS), describe whether each mutagen would be able to revert these codons to wild type

Solution

EMS induces primarily G · C → A · T transitions. UAG codons could not be reverted to wild type because only the UAG → UAA change would be stimulated by EMS and that generates a nonsense (ochre) codon. UAA codons would not be acted on by EMS. Aflatoxin B₁ induces primarily G · C → T · A transversions. Only the third position of UAG codons would be acted on, resulting in a UAG → UAU change (on the mRNA level), which produces tyrosine. Therefore, if tyrosine were an acceptable amino acid at the corresponding site in the protein, aflatoxin B1 could revert UAG codons. Aflatoxin B1 would not revert UAA codons because no G · C base pairs appear at the corresponding position in the DNA.

SOLVED PROBLEM 2. Explain why mutations induced by acridines in phage T4 or by ICR-191 in bacteria cannot be reverted by 5-bromouracil.

Solution

Acridines and ICR-191 induce mutations by deleting or adding one or more base pairs, which results in a frameshift. However, 5-bromouracil induces mutations by causing the substitution of one base for another. This substitution cannot compensate for the frameshift resulting from ICR-191 and acridines.