Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1993 Sep;240(3):360-4.
doi: 10.1007/BF00280387.

The pleiotropic effects of his overexpression in Salmonella typhimurium do not involve AICAR-induced mutagenesis

Affiliations

The pleiotropic effects of his overexpression in Salmonella typhimurium do not involve AICAR-induced mutagenesis

A Flores et al. Mol Gen Genet. 1993 Sep.

Abstract

Inhibition of cell division associated with overexpression of hisH and hisF in Salmonella typhimurium is strongly reminiscent of a cellular response to DNA damage. On these grounds, we investigated the involvement of a metabolite which appeared to represent a possible candidate for an endogenous mutagen: the base analog 5-amino-4-carboxamide imidazole riboside 5'-phosphate (AICAR), a by-product of HisH and HisF activity. However, we showed that AICAR is not an endogenous mutagen in S. typhimurium. Other types of DNA damage induced by his overexpression seem also unlikely, since similar mutation rates are found in hisO+ and hisOc strains. We also show that AICAR production is not involved in the pleiotropic effects of his overexpression, since these are still observed in strains devoid of AICAR. Thus inhibition of cell division resulting from HisH and HisF overexpression must operate through a mechanism unrelated to the role of these proteins in histidine biosynthesis.

PubMed Disclaimer

References

    1. J Bacteriol. 1979 Mar;137(3):1271-81 - PubMed
    1. J Bacteriol. 1983 Feb;153(2):1114-9 - PubMed
    1. J Bacteriol. 1981 Sep;147(3):827-35 - PubMed
    1. J Biol Chem. 1956 Jan;218(1):97-106 - PubMed
    1. J Mol Biol. 1967 Nov 28;30(1):81-95 - PubMed

LinkOut - more resources