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FEMS Microbiol Lett. 2012 Jun;331(2):136-43. doi: 10.1111/j.1574-6968.2012.02564.x. Epub 2012 Apr 30.

Binding of the IclR-type regulator HutR in the histidine utilization (hut) gene cluster of the human pathogen Corynebacterium resistens DSM 45100.

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  • 1Institute for Genome Research and Systems Biology, Center for Biotechnology, Bielefeld University, Bielefeld, Germany.

Abstract

The genome of the human pathogen Corynebacterium resistens DSM 45100 is equipped with a histidine utilization (hut) gene cluster encoding a four-step pathway for the catabolism of l-histidine and a transcriptional regulator of the IclR superfamily, now named HutR. The utilization of l-histidine might be relevant for the growth of C. resistens in its natural habitat, probably the histidine-rich inguinal and perineal areas of the human body. The ability of C. resistens to utilize l-histidine as a sole source of nitrogen was demonstrated by growth assays in synthetic minimal media. Reverse transcriptase PCRs revealed enhanced transcript levels of the hut genes in C. resistens cells grown in the presence of l-histidine. Promoter-probe assays showed that the hut genes are organized in three transcription units: hutHUI, hutR, and hutG. The respective transcriptional start sites were mapped by 5' RACE-PCR to detected putative promoter regions. DNA band shift assays with purified HutR protein identified the 14-bp DNA sequence TCTGwwATwCCAGA located upstream of the mapped promoters. This DNA motif includes a 4-bp terminal palindrome, which turned out to be essential for HutR binding in vitro. These data add a new physiological function to the large IclR family of transcriptional regulators.

© 2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved.

PMID:
22462578
[PubMed - indexed for MEDLINE]
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