A hotspot for spontaneous frameshift mutations in the histidinol dehydrogenase gene of Salmonella typhimurium |
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| Authors: | J Yourno I Ino T Kono |
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| Affiliation: | 2. Center for Biodefense and Emerging Infectious Diseases, The University of Texas Medical Branch, Galveston, TX, United States;3. UTMB Center for Tropical Diseases, The University of Texas Medical Branch, Galveston, TX, United States;4. Sealy Center for Vaccine Development, The University of Texas Medical Branch, Galveston, TX, United States;5. Institute for Human Infections and Immunity, The University of Texas Medical Branch, Galveston, TX, United States;1. Research team, Pathophysiology and Epidemiology of Cerebro-Cardiovascular diseases (PEC2, EA 7460), University of Bourgogne Franche-Comté, UFR des Sciences de Santé, 7 boulevard Jeanne d’ Arc, 21079 DIJON, France;2. Cardiology Unit, Dijon University Hospital Center, Dijon, France |
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| Abstract: | A hotspot for spontaneous frameshift mutations in the histidinol dehydrogenase gene of Salmonella typhimurium contains two radically different types of frameshift. Reversion of each type occurs spontaneously but is not enhanced by the frameshift mutagens tested. One type, interpreted as extensive deletions, reverts at a very low frequency and produces only pseudo-wild type (+−) revertants in which histidinol dehydrogenase is either undetectable or cold-sensitive in vitro. The other type of frameshift, interpreted as duplications, reverts at a very high frequency and yields only apparently wild-type revertants with normal histidinol dehydrogenase. Neither type of frameshift appears to be externally suppressible. The hotspot contains a repeating DNA sequence of two to three G.C pairs and occasionally yields (+1) frameshift mutations with the acridine derivative, ICR-191, presumably by strand slippage. Slippage of greater extent may generate the complex spontaneous lesions. |
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