Overexpression of sigma factor, sigma(B), urges Staphylococcus aureus to thicken the cell wall and to resist beta-lactams.
Whole genome sequence analysis revealed that Staphylococcus aureus is provided with only a few sigma factors, including the alternative sigma factor, sigma(B), which is thought to regulate some stress responses. Since the sigB knock-out mutant did not show remarkable phenotypic difference, we constructed the over expressed mutant to examine the role of the sigB. Electron microscopic observation revealed that the mutant showed a variety of cell sizes compared with the parent strain which showed almost homogeneous cell sizes. The mutant delivered a thicker cell wall, about 20% thicker than the parent strain. It became resistant to the lytic activity of lysostaphin and also raised MICs to the cell-wall-affecting antibiotics. The yield of carotenoids and transcripts of pbps were also increased in the mutant. The result suggests that sigB plays some important roles in cell wall synthesis and in resistance to antibiotics that perturb the cell wall synthesis.
Morikawa
K
K
College of Medical Technology, University of Tsukuba, Tsukuba, 305-8577 Japan.
Maruyama
A
A
Inose
Y
Y
Higashide
M
M
Hayashi
H
H
Ohta
T
T
D001426:Bacterial Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D002473:Cell Wall / Q000502:physiology*; D004351:Drug Resistance / Q000502:physiology; D012808:Sigma Factor / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D013211:Staphylococcus aureus / Q000187:drug effects / Q000502:physiology*; D047090:beta-Lactams / Q000494:pharmacology
D001426:Bacterial Proteins; C079011:SigB protein, Bacteria; D012808:Sigma Factor; D047090:beta-Lactams