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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Gene Review

hemB  -  delta-aminolevulinic acid dehydratase

Staphylococcus aureus RF122

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Disease relevance of hemB

  • Staphylococcus aureus menD and hemB mutants are as infective as the parent strains, but the menadione biosynthetic mutant persists within the kidney [1].
  • In this study, DNA array transcriptional profiles of clinical SCVs isolated from the airways of cystic fibrosis patients were obtained and compared to those obtained from a laboratory-derived SCV strain (i.e., a respiratory-deficient hemB mutant) and prototype S. aureus strains [2].
  • The aim of this study was to assess the virulence of an hemB mutant, which has been shown to display the typical characteristics of clinical SCVs, in a murine model of septic arthritis [3].
  • An hemB deletion mutant of S. aureus Newbould, a bovine mastitis isolate, having a stable, genetically defined SCV phenotype, was used in a screening program to identify compounds active against intracellular, gram-positive bacteria [4].

High impact information on hemB

  • In this study, we show that clinical SCVs as well as hemB- and menD-deficient mutants of S. aureus are greatly reduced in virulence in the C. elegans infection model [5].
  • No differences were observed between the response of the hemB mutant to oxacillin therapy and that of the parent strain in any target tissues, and significant reductions in bacterial densities were seen in all tissues (compared with untreated controls) [1].
  • Small colony variants (SCVs) of Staphylococcus aureus were generated via mutations in menD or hemB, yielding menadione and hemin auxotrophs, respectively, and studied in the rabbit endocarditis model [1].
  • Real-time quantitative reverse transcription-PCR demonstrated increased expression of clfA and fnb genes by the hemB mutant compared to its isogenic parent [6].
  • Increased expression of clumping factor and fibronectin-binding proteins by hemB mutants of Staphylococcus aureus expressing small colony variant phenotypes [6].

Biological context of hemB

  • Compared to parent strain COL, the hemB mutant was defective in utilization of a variety of carbon sources, including Krebs cycle intermediates and compounds that ultimately generate ATP via electron transport [7].
  • The genes commonly up-regulated in both hemB and clinical SCVs were found to be implicated in fermentation and glycolysis pathways [2].
  • These results strongly indicate that the hemB mutant generates ATP from glucose or fructose only by substrate phosphorylation [8].

Anatomical context of hemB

  • These results suggest that, although the hemB mutant has a reduced ability to colonize mammary glands, the SCV phenotype may account for the persistence of S. aureus under antibiotic pressure in vivo [9].
  • The hemB mutant was phagocytosed by cultured endothelial cells, but did not lyse these cells, because the mutant produced very little alpha-toxin [10].

Associations of hemB with chemical compounds

  • Transcriptional analysis of citB, encoding the aconitase, revealed that the activity of the citrate cycle enzymes was down-regulated in the hemB mutant [8].
  • We studied four SCVs and their corresponding parent strains: one clinical strain pair, one menaquinone-deficient spontaneous mutant, and two constructed mutants obtained by inactivation of hemB in S. aureus 8325-4 and COL, respectively [11].
  • However, although the hemB mutant was as susceptible as S. aureus Newbould to cephapirin in vitro, it was over a 100 times more persistent than the parental strain in the mammary glands when 1 or 2 mg kg(-1) doses were administrated [9].

Other interactions of hemB

  • Results showed that clinical SCVs persisted much more efficiently in cells than the hemB and prototype strains and that a sigB mutant was a poor persister [2].

Analytical, diagnostic and therapeutic context of hemB


  1. Staphylococcus aureus menD and hemB mutants are as infective as the parent strains, but the menadione biosynthetic mutant persists within the kidney. Bates, D.M., von Eiff, C., McNamara, P.J., Peters, G., Yeaman, M.R., Bayer, A.S., Proctor, R.A. J. Infect. Dis. (2003) [Pubmed]
  2. Transcription of virulence factors in Staphylococcus aureus small-colony variants isolated from cystic fibrosis patients is influenced by SigB. Moisan, H., Brouillette, E., Jacob, C.L., Langlois-Bégin, P., Michaud, S., Malouin, F. J. Bacteriol. (2006) [Pubmed]
  3. Virulence of a hemB mutant displaying the phenotype of a Staphylococcus aureus small colony variant in a murine model of septic arthritis. Jonsson, I.M., von Eiff, C., Proctor, R.A., Peters, G., Rydén, C., Tarkowski, A. Microb. Pathog. (2003) [Pubmed]
  4. Identification of antimicrobial compounds active against intracellular Staphylococcus aureus. Malouin, F., Brouillette, E., Martinez, A., Boyll, B.J., Toth, J.L., Gage, J.L., Allen, N.E. FEMS Immunol. Med. Microbiol. (2005) [Pubmed]
  5. Virulence of Staphylococcus aureus small colony variants in the Caenorhabditis elegans infection model. Sifri, C.D., Baresch-Bernal, A., Calderwood, S.B., von Eiff, C. Infect. Immun. (2006) [Pubmed]
  6. Increased expression of clumping factor and fibronectin-binding proteins by hemB mutants of Staphylococcus aureus expressing small colony variant phenotypes. Vaudaux, P., Francois, P., Bisognano, C., Kelley, W.L., Lew, D.P., Schrenzel, J., Proctor, R.A., McNamara, P.J., Peters, G., Von Eiff, C. Infect. Immun. (2002) [Pubmed]
  7. Phenotype microarray profiling of Staphylococcus aureus menD and hemB mutants with the small-colony-variant phenotype. von Eiff, C., McNamara, P., Becker, K., Bates, D., Lei, X.H., Ziman, M., Bochner, B.R., Peters, G., Proctor, R.A. J. Bacteriol. (2006) [Pubmed]
  8. Physiological characterization of a heme-deficient mutant of Staphylococcus aureus by a proteomic approach. Kohler, C., von Eiff, C., Peters, G., Proctor, R.A., Hecker, M., Engelmann, S. J. Bacteriol. (2003) [Pubmed]
  9. Persistence of a Staphylococcus aureus small-colony variant under antibiotic pressure in vivo. Brouillette, E., Martinez, A., Boyll, B.J., Allen, N.E., Malouin, F. FEMS Immunol. Med. Microbiol. (2004) [Pubmed]
  10. Staphylococcus aureus small colony variants: formation and clinical impact. von Eiff, C., Proctor, R.A., Peters, G. International journal of clinical practice. Supplement. (2000) [Pubmed]
  11. Physiology and antibiotic susceptibility of Staphylococcus aureus small colony variants. Baumert, N., von Eiff, C., Schaaff, F., Peters, G., Proctor, R.A., Sahl, H.G. Microb. Drug Resist. (2002) [Pubmed]
  12. Staphylococcus aureus small colony variants are resistant to the antimicrobial peptide lactoferricin B. Samuelsen, O., Haukland, H.H., Kahl, B.C., von Eiff, C., Proctor, R.A., Ulvatne, H., Sandvik, K., Vorland, L.H. J. Antimicrob. Chemother. (2005) [Pubmed]
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