Altered gene expression in the transition phase by disruption of a Na+/H+ antiporter gene (shaA) in Bacillus subtilis.
The shaA gene (sodium-hydrogen antiporter gene A, identical to mrpA) is largely responsible for Na+ extrusion in Bacillus subtilis. The disruption of shaA combined with a low concentration of NaCl completely abolishes sporulation but allows normal growth. To investigate the role of shaA and shaA-mediated sodium ion homeostasis in sporulation, we performed a comprehensive study of expression profiles of eight alternative sigma factors, sigmaB and the seven extracytoplasmic function sigma factors (sigmaM, sigmaV, sigmaW, sigmaX, sigmaY, sigmaZ, and sigmaYlaC) in an attempt to determine the global change of gene expression that results from a disturbance of Na+ homeostasis caused by shaA disruption. Induction of sigmaB activity in the transition phase was impaired in the shaA mutant, and this effect was enhanced in the presence of 30 mM NaCl. Salt stress activation of sigmaB occurred normally in the shaA mutant. sigmaM-, sigmaW-, sigmaX-dependent transcription and sigZ transcription was also induced in the transition phase of the wild-type, which was modulated by shaA disruption. The induction of sigmaM-dependent transcription was enhanced in the shaA mutant, while that of sigmaX-dependent transcription and sigZ transcription was decreased. sigmaW-dependent transcription was increased throughout the growth phase of the shaA mutant, which was consistent with the result of proteome analysis. We conclude that shaA disruption resulted in the modulated induction of alternative sigma factor activities, which would be problematic for the cell upon entering the sporulation stage.
Kosono
Saori
S
Saitama University, Saitama City, Saitama 338-8570, Japan. kosono@riken.jp
Asai
Kei
K
Sadaie
Yoshito
Y
Kudo
Toshiaki
T
D019677:Artificial Gene Fusion; D001412:Bacillus subtilis / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism*; D001426:Bacterial Proteins / Q000032:analysis / Q000096:biosynthesis* / Q000235:genetics; D015964:Gene Expression Regulation, Bacterial / Q000502:physiology; D005798:Genes, Bacterial; D017930:Genes, Reporter; D007763:Lac Operon / Q000235:genetics; D020543:Proteome / Q000032:analysis; D012808:Sigma Factor / Q000096:biosynthesis* / Q000235:genetics; D012965:Sodium Chloride / Q000378:metabolism; D017923:Sodium-Hydrogen Exchangers / Q000235:genetics* / Q000502:physiology*; D013171:Spores, Bacterial / Q000235:genetics / Q000254:growth & development; D001616:beta-Galactosidase / Q000235:genetics / Q000378:metabolism
D001426:Bacterial Proteins; D020543:Proteome; C079011:SigB protein, Bacteria; D012808:Sigma Factor; D017923:Sodium-Hydrogen Exchangers; D012965:Sodium Chloride; D001616:beta-Galactosidase