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Sulfate Metabolism in Mycobacteria
Author(s) -
Schelle Michael W.,
Bertozzi Carolyn R.
Publication year - 2006
Publication title -
chembiochem
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.05
H-Index - 126
eISSN - 1439-7633
pISSN - 1439-4227
DOI - 10.1002/cbic.200600224
Subject(s) - sulfation , biology , mycobacterium tuberculosis , bacteria , microbiology and biotechnology , assimilation (phonology) , metabolite , sulfur metabolism , human pathogen , virulence , pathogenic bacteria , tuberculosis , immune system , mycobacterium , biochemistry , enzyme , gene , genetics , medicine , linguistics , philosophy , pathology
Pathogenic bacteria have developed numerous mechanisms to survive inside a hostile host environment. The human pathogen Mycobacterium tuberculosis ( M. tb ) is thought to control the human immune response with diverse biomolecules, including a variety of exotic lipids. One prevalent M. tb ‐specific sulfated metabolite, termed sulfolipid‐1 (SL‐1), has been correlated with virulence though its specific biological function is not known. Recent advances in our understanding of SL‐1 biosynthesis will help elucidate the role of this curious metabolite in M. tb infection. Furthermore, the study of SL‐1 has led to questions regarding the significance of sulfation in mycobacteria. Examples of sulfated metabolites as mediators of interactions between bacteria and plants suggest that sulfation is a key modulator of extracellular signaling between prokaryotes and eukaryotes. The discovery of novel sulfated metabolites in M. tb and related mycobacteria strengthens this hypothesis. Finally, mechanistic and structural data from sulfate‐assimilation enzymes have revealed how M. tb controls the flux of sulfate in the cell. Mutants with defects in sulfate assimilation indicate that the fate of sulfur in M. tb is a critical survival determinant for the bacteria during infection and suggest novel targets for tuberculosis drug therapy.