A glutamate-alanine-leucine (EAL) domain protein of Salmonella controls bacterial survival in mice, antioxidant defence and killing of macrophages:: role of cyclic diGMP

被引：113

作者：

Hisert, KB

MacCoss, M

Shiloh, MU

Darwin, KH

Singh, S

Jones, RA

Ehrt, S

Zhang, ZY

Gaffney, BL

Gandotra, S

Holden, DW

Murray, D ^{[1
]}

Nathan, C

机构：

[1] Cornell Univ, Weill Med Coll, Dept Microbiol & Immunol, New York, NY 10021 USA

[2] Cornell Univ, Weill Grad Sch Med Sci, Program Immunol & Microbial Pathogenesis, New York, NY USA

[3] Cornell Univ, Weill Grad Sch Med Sci, Program Mol Biol, New York, NY USA

[4] Cornell Univ, Weill Grad Sch Med Sci, Program Struct Biol Biochem, New York, NY USA

[5] Univ Washington, Dept Genome Sci, Seattle, WA 98195 USA

[6] Rutgers State Univ, Dept Chem & Biol Chem, Piscataway, NJ USA

[7] Univ London Imperial Coll Sci Technol & Med, Ctr Mol Microbiol & Infect, London, England

来源：

MOLECULAR MICROBIOLOGY | 2005年 / 56卷 / 05期

关键词：

D O I：

10.1111/j.1365-2958.2005.04632.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Signature-tagged transposon mutagenesis of Salmonella with differential recovery from wild-type and immunodeficient mice revealed that the gene here named cdgR[for c-diguanylate (c-diGMP) regulator] is required for the bacterium to resist host phagocyte oxidase in vivo. CdgR consists solely of a glutamate-alanine-leucine (EAL) domain, a predicted cyclic diGMP (c-diGMP) phosphodiesterase. Disruption of cdgR decreased bacterial resistance to hydrogen peroxide and accelerated bacterial killing of macrophages. An ultrasensitive assay revealed c-diGMP in wild-type Salmonella with increased levels in the CdgR-deficient mutant. Thus, besides its known role in regulating cellulose synthesis and biofilm formation, bacterial c-diGMP also regulates host-pathogen interactions involving antioxidant defence and cytotoxicity.

引用

页码：1234 / 1245

页数：12

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