A novel regulatory protein governing biofilm formation in Bacillus subtilis

Molecular Microbiology (2008) 68(5), 1117-1127

Speaker: 謝政原                          Time:14:10~15:00, Oct. 22, 2008

Commentator: 吳俊忠 老師                Place: Room 601

Abstract:

Most of the wild strains of a spore-forming bacterium, Bacillus subtilis, form robust floating biofilms (pellicle) in the liquid medium and exhibit complex colony structure on the solid medium. The extracellular matrix of B. subtilis biofilm is composed of the exopolysaccharide encoded by theepsA-O operon and the protein encoded by tasA, a gene in the yqxM operon. It has been shown that SinR represses the transcription of both operons. The expression of SinR is repressed by SinI, which is activated by the transcription factor Spo0A. On the other hand, mutation of abrB, a transcription regulator, can restore the biofilm formation of a spo0A mutant, suggesting that AbrB is a repressor of several genes in biofilm formation. In this study, the authors further identified the potential targets of AbrB and inverstigated the relative contributions of AbrB and SinR to controlling the expression of these operons. The hyper-wrinkled phenotype of the abrB mutant was similar to that of the sinR mutant, and the abrB mutant overexpressed the lacZ gene fused to P_eps and P_yqxM. However, abrB mutant did not show increased expression of the lacZ gene fused to P_sinI, indicating that SinI was not under the control of AbrB. By comparing the expression levels of eps and yqxM operons in the single and double mutants of abrB and sinR, they found that ArbB repressed mainly the eps operon while SinR repressed mainly the yqxM operon. The authors futher confirmed that AbrB bound to P_yqxMbut not P_eps. While they were identifying the AbrB-binding sequence in P_yqxM, they found that two identical direct repeat sequences downstream of the AbrB-binding site were required for the transcription of yqxM operon, suggesting that an activator may be involved in the activation of this operon. By bioinformatic analysis, they selected Slr, a SinR-like protein as a candidate of the activator. They found that Slr indeed stimulates the transcption of P_yqxM. Both of abrB and sinR repressed the transcription of slr, with the latter playing a major role. In summary, the matrix production is repressed by AbrB and SinR independently and activated by a novel protein, Slr, which is also repressed by AbrB and SinR.

References:

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