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  Urocanate as a potential signaling molecule for bacterial recognition of eukaryotic hosts

Zhang, X.-X., Ritchie, S. R., & Rainey, P. B. (2014). Urocanate as a potential signaling molecule for bacterial recognition of eukaryotic hosts. Cellular and Molecular Life Sciences, 71(4), 541-547. doi:10.1007/s00018-013-1527-6.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0014-C5F1-C Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0015-83C1-C
Genre: Journal Article

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 Creators:
Zhang, Xue-Xian, Author
Ritchie, Stephen R., Author
Rainey, Paul B.1, Author              
Affiliations:
1External Scientific Member Group Experimental and Evolutionary Genetics, Max Planck Institute for Evolutionary Biology, Max Planck Society, ou_1445637              

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Free keywords: urocanic acid; host perception; infectious diseases; histidine utilization; HutC; Pseudomonas
 Abstract: Host recognition is the crucial first step in infectious disease pathogenesis. Recognition allows pathogenic bacteria to identify suitable niches and deploy appropriate phenotypes for successful colonization and immune evasion. However, the mechanisms underlying host recognition remain largely unknown. Mounting evidence suggests that urocanate—an intermediate of the histidine degradation pathway—accumulates in tissues, such as skin, and acts as a molecule that promotes bacterial infection via molecular interaction with the bacterial regulatory protein HutC. In Gram-negative bacteria, HutC has long been known as a transcriptional repressor of hut genes for the utilization of histidine (and urocanate) as sources of carbon and nitrogen. Recent work on the opportunistic human pathogen Pseudomonas aeruginosa and zoonotic pathogen Brucella abortus shows that urocanate, in conjunction with HutC, plays a significant role in the global control of cellular metabolism, cell motility, and expression of virulence factors. We suggest that in addition to being a valuable source of carbon and nitrogen, urocanate may be central to the elicitation of bacterial pathogenesis.

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Language(s): eng - English
 Dates: 2013-10-292013-09-092013-11-182013-12-052014-02
 Publication Status: Published in print
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 Identifiers: DOI: 10.1007/s00018-013-1527-6
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Title: Cellular and Molecular Life Sciences
Source Genre: Journal
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Publ. Info: Springer
Pages: - Volume / Issue: 71 (4) Sequence Number: - Start / End Page: 541 - 547 Identifier: ISSN: 1420-682X (print)
ISSN: 0014-4754 (print)
ISSN: 1420-9071 (online)
CoNE: /journals/resource/954926942730