Synthetic Lethality of the <i>bfr</i> and <i>mbfA</i> Genes Reveals a Functional Relationship between Iron Storage and Iron Export in Managing Stress Responses in <i>Bradyrhizobium japonicum</i>


<div><p>An <i>mbfA</i> mutant of <i>Bradyrhizobium japonicum</i> defective in iron export is sensitive to short term exposure to high levels iron or H<sub>2</sub>O<sub>2</sub>. Here, we found that the <i>mbfA</i> strain grown in elevated iron media (100 μM) became resistant to those treatments, suggesting a stress response adaptation. The <i>bfr</i> gene encodes the iron storage protein bacterioferritin, and its expression is derepressed by iron. An <i>mbfA bfr</i> double mutant showed a loss of stress adaptation, and had a severe growth phenotype in high iron media. Moreover, a <i>bfr</i><sup><i>up</i></sup> allele in which <i>bfr</i> is constitutively derepressed conferred stress tolerance on an <i>mbfA</i> mutant without elevating the iron content in the growth media. The intracellular iron content of the <i>mbfA bfr</i> double mutant was substantially higher than that found in the wild type, even when grown in relatively low iron media (5 μM). Under that condition, iron-responsive gene expression was aberrant in the <i>mbfA bfr</i> strain. Moreover, the double mutant was sensitive to the iron-activated antibiotic streptonigrin. We conclude that MbfA and Bfr work in concert to manage iron and oxidative stresses. In addition, the need for iron detoxification is not limited to extreme environments, but is also required for normal cellular function.</p></div

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oai:figshare.com:article/3434327Last time updated on 2/12/2018

This paper was published in FigShare.

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