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Transcriptomic buffering of cryptic genetic variation contributes to meningococcal virulence
Biju Joseph Ampattu1, Laura Hagmann1, Chunguang Liang2
1Institute for Hygiene and Microbiology, Joseph-Schneider-Straße 2, University of Würzburg, 97080, Würzburg, Germany.
BMC Genomics
|April 9, 2017
Summary
Neisseria meningitidis virulence is linked to gene regulation, not just genetic differences. Transcriptional control of metabolic genes and stress responses influences bacterial disease potential.
Area of Science:
- Microbiology
- Genomics
- Systems Biology
Background:
- Neisseria meningitidis can transition from commensal to pathogenic.
- Genomic comparisons have not clearly identified key virulence factors.
- Understanding gene regulation is crucial for meningococcal virulence.
Purpose of the Study:
- Compare gene expression between invasive and carriage strains of N. meningitidis.
- Investigate the role of gene regulation in meningococcal virulence.
- Assess strain-specific gene expression under conditions mimicking host environments.
Main Methods:
- Systems biology approach comparing gene expression.
- Ex vivo culture conditions mimicking commensal and virulence environments.
- Transcriptomic analysis and computational modeling.
Main Results:
- Over 500 genes differed in expression between strains under infection-mimicking conditions.
- Differences observed in metabolic, information processing, and host-damage related genes (e.g., nitrite reductase, LOS biosynthesis).
- Computational models predicted metabolic flux differences and stringent response activation; experimental data confirmed auxotrophies and essentiality of relA gene.
Conclusions:
- Meningococcal virulence is associated with transcriptional buffering of metabolic gene variations and stress responses.
- Regulatory elements play a significant role in bacterial virulence.
- Model strain approaches have limitations for studying genetically diverse bacteria like N. meningitidis.