Deletion of the hmc operon of Desulfovibrio vulgaris subsp vulgaris Hildenborough hampers hydrogen metabolism and low-redox-potential niche establishment

The hmc operon of Desulfovibrio vulgaris subsp. vulgaris Hildenborough enco des a transmembrane redox protein complex (the Hmc complex) that has been p roposed to catalyze electron transport linking periplasmic hydrogen oxidati on to cytoplasmic sulfate reduction. We have replaced a 5-kb DNA fragment c ontaining most of the hmc operon by the cat gene. The resulting chloramphen icol-resistant mutant D. vulgaris H801 grows normally when lactate or pyruv ate serve as electron donors for sulfate reduction. Growth with hydrogen as electron donor for sulfate reduction (acetate and co, as the carbon source ) is impaired. These results confirm the importance of the Hmc complex in e lectron transport from hydrogen to sulfate. Mutant H801 is also deficient i n low-redox-potential niche establishment. On plates, colony development ta kes 14 days longer than colony development of the wild-type strain, when th e cells use hydrogen as the electron donor. This result suggests that, in a ddition to transmembrane electron transport from hydrogen to sulfate, the r edox reactions catalyzed by the Hmc complex are crucial in establishment of the required low-redox-potential niche that allows single cells to grow in to colonies.