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Published on: February 19, 2019
SppR in Streptococcus mutans coordinates stress tolerance response and BrpA expression
Zezhang T Wen1,2, Bo Yang1, Lauren C Guillot1
1Department of Oral and Craniofacial Biology, Louisiana State University Health School of Dentistry, New Orleans, LA, United States.
The transcriptional repressor SppR is crucial for Streptococcus mutans stress tolerance. SppR deficiency impairs growth at low pH and under oxidative stress, impacting biofilm formation and gene regulation.
Area of Science:
- Microbiology
- Molecular Biology
- Genetics
Background:
- SppR acts as a transcriptional repressor for fructanase (FruA) and fructose-1-phosphatase (SppA).
- Understanding SppR's role is vital for addressing *Streptococcus mutans* physiology, particularly its resilience to environmental stressors.
Purpose of the Study:
- To investigate the function of SppR in *S. mutans* stress tolerance and biofilm formation.
- To elucidate SppR's regulatory role in *brpA* gene expression.
Main Methods:
- Construction and analysis of a frameshift *sppR* mutant using *in vitro* biofilm models and stress challenge assays.
- Luciferase reporter fusion assays and *in vitro* transcription assays to study *brpA* regulation.
- RNA-sequencing (RNA-seq) to analyze global gene expression changes in the *sppR* mutant.
Main Results:
- *sppR* deficiency negatively impacted growth at low pH and under oxidative stress, reducing survival rates.
- SppR represses *brpA* expression, evidenced by reduced promoter activity in the mutant and direct binding of recombinant SppR to the *brpA* promoter.
- RNA-seq revealed altered expression of over 136 genes in the *sppR* mutant, including those involved in DNA repair and acid tolerance.
Conclusions:
- SppR is essential for *S. mutans*' acid and oxidative stress tolerance.
- SppR plays a significant role in regulating *brpA* expression, contributing to the bacterium's overall physiology and stress response.
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