Complete genome of the thermophilic purple sulfur Bacterium Thermochromatium tepidum compared to Allochromatium vinosum and other Chromatiaceae.

The complete genome sequence of the thermophilic purple sulfur bacterium Thermochromatium tepidum strain MCT (DSM 3771T) is described and contrasted with that of its mesophilic relative Allochromatium vinosum strain D (DSM 180T) and other Chromatiaceae. The Tch. tepidum genome is a single circular chromosome of 2,958,290 base pairs with no plasmids and is substantially smaller than the genome of Alc. vinosum. The Tch. tepidum genome encodes two forms of RuBisCO and contains nifHDK and several other genes encoding a molybdenum nitrogenase but lacks a gene encoding a protein that assembles the Fe-S cluster required to form a functional nitrogenase molybdenum-iron cofactor, leaving the phototroph phenotypically Nif-. Tch. tepidum contains genes necessary for oxidizing sulfide to sulfate as photosynthetic electron donor but is genetically unequipped to either oxidize thiosulfate as an electron donor or carry out assimilative sulfate reduction, both of which are physiological hallmarks of Alc. vinosum. Also unlike Alc. vinosum, Tch. tepidum is obligately phototrophic and unable to grow chemotrophically in darkness by respiration. Several genes present in the Alc. vinosum genome that are absent from the genome of Tch. tepidum likely contribute to the major physiological differences observed between these related purple sulfur bacteria that inhabit distinct ecological niches.

Slow and steady wins the race: an examination of bacterial persistence.

Bacterial persistence is a state of metabolic dormancy among a small fraction (<1%) of a genetically identical population of cells that, as a result, becomes transiently resistant to environmental stressors. Such cells, called persisters, are able to survive indeterminate periods of exposure to challenging and even hostile environmental conditions, including nutrient deprivation, oxidative stress, or the presence of an antibiotic to which the bacterium would normally be susceptible. Subpopulations of cells having the persister phenotype is also a common feature of biofilms, in which limited space, hypoxia, and nutrient deficiencies all contribute to the onset of persistence. Microbiologists have been aware of bacterial persistence since the early days of antibiotic development. However, in recent years the significance of this phenomenon has been brought into new focus, as persistent bacterial infections that require multiple rounds of antibiotic treatment are becoming a more widespread clinical challenge. Here, we provide an overview of the major features of bacterial persistence, including the various conditions that precipitate persister formation and a discussion of several of the better-characterized molecular mechanisms that trigger this distinctive mode of bacterial dormancy.