[Early management of cerebral movement disorders].
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Biomedical subjects
Publications and source records attributed to H Berger.
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Frameshift mutant trpA21 was isolated after ultraviolet treatment and frameshift mutant trpA540 after ICR191-A (an acridine derivative) treatment of wild-type Escherichia coli K-12. The A proteins of spontaneous and ICR191-A-induced partial revertants of these mutants contained altered amino acid sequences one residue shorter than the comparable sequence in the A protein of wild-type bacteria. The data support the conclusion that ICR191-A causes frameshift mutations. The findings further indicate that both base additions and deletions are elicited by ICR191-A treatment and that mutagenesis by this compound sometimes affects more than one base pair. ICR191-A also weakly reverts some missense mutants. Analyses of the relevant peptides of the purified A protein show single amino acid replacements compatible with single base-pair changes. In addition, we found that some spontaneously revertible ICR191-A- and ultraviolet light-induced frameshift mutants are not further stimulated to revert by exposure to ultraviolet light.
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In studies with A protein mutants of the tryptophan synthetase of Escherichia coli, missense supressors have been used to select for codon changes and corresponding amino acid replacements that are normally unobservable. The technique has permitted the detection of additional amino acid replacements expected on the basis of the genetic code.
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