Cobalt targets multiple metabolic processes in Salmonella enterica.

Abstract:

:Cobalt is essential for growth of Salmonella enterica and other organisms, yet this metal can be toxic when present in excess. Wild-type Salmonella exhibits several metabolic defects when grown in the presence of cobalt, some of which generate visible growth consequences. Work herein identifies sulfur assimilation, iron homeostasis, and Fe-S cluster metabolism as targets for cobalt toxicity. In each case it is proposed that cobalt exerts its effect by one of two mechanisms: direct competition with iron or indirectly through a mechanism that involves the status of reduced thiols in the cell. Cobalt toxicity results in decreased siroheme production, increased expression of the Fur regulon, and decreased activity of Fe-S cluster proteins. The consequences of reduced sulfite reductase activity in particular are exacerbated by the need for glutathione in cobalt resistance. Significantly, independent metabolic perturbations could be detected at cobalt concentrations below those required to generate a detectable growth defect.

journal_name

J Bacteriol

journal_title

Journal of bacteriology

authors

Thorgersen MP,Downs DM

doi

10.1128/JB.00962-07

subject

Has Abstract

pub_date

2007-11-01 00:00:00

pages

7774-81

issue

21

eissn

0021-9193

issn

1098-5530

pii

JB.00962-07

journal_volume

189

pub_type

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