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Coexpression patterns of sigma(B) regulators in Bacillus subtilis affect sigma(B) inducibility
Shuyu Zhang1, Adam Reeves, Robyn L Woodbury
1Department of Microbiology and Immunology, MC7758, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA. zhangs@UTHSCSA.EDU
Coexpression of RsbT with adjacent genes, RsbS and RsbU, is crucial for activating the Bacillus subtilis sigma(B) transcription factor under stress. Proper gene arrangement ensures RsbT function, highlighting the importance of operon structure in stress response.
Area of Science:
- Microbiology
- Molecular Biology
- Bacterial Stress Response
Background:
- RsbT is vital for activating the Bacillus subtilis sigma(B) transcription factor during physical stress.
- The rsbT gene is part of an operon with its regulator RsbS and target RsbU.
- Gene proximity and coexpression significantly impact RsbT's regulatory function.
Purpose of the Study:
- To investigate the influence of coexpression with adjacent genes (rsbS and rsbU) on RsbT function.
- To determine the role of operon structure in the stress-activated sigma(B) pathway.
- To elucidate the interaction between RsbS and RsbT in regulating sigma(B) activity.
Main Methods:
- Genetic manipulation to express rsbT at sites separate from rsbS and rsbU.
- Construction of merodiploid strains to study allelic interactions.
- Analysis of sigma(B) activation following stress induction in various genetic contexts.
Main Results:
- Displaced expression of rsbT leads to non-functional RsbT, despite accumulation.
- RsbT activity is restored when rsbT is cotranscribed with rsbS and rsbU.
- Constitutive RsbS activity is dependent on cotranscription with rsbT and exhibits complex dominance relationships.
Conclusions:
- Coexpression and operon organization are critical for RsbT's ability to activate sigma(B).
- RsbS and RsbT likely form stable complexes upon co-synthesis, maintaining RsbT in a stress-activatable state.
- The spatial arrangement of genes within an operon is essential for efficient signal transduction in bacterial stress response pathways.
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