PNEUMOCELL
Noise in gene expression as a determinant of virulence of the human pathogen Streptococcus pneumoniae
| Coordinatore | RIJKSUNIVERSITEIT GRONINGEN
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | Netherlands [NL] |
| Totale costo | 1˙498˙846 € |
| EC contributo | 1˙498˙846 € |
| Programma | FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | ERC-2013-StG |
| Funding Scheme | ERC-SG |
| Anno di inizio | 2013 |
| Periodo (anno-mese-giorno) | 2013-11-01 - 2018-10-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
RIJKSUNIVERSITEIT GRONINGEN
Organization address
address: Broerstraat 5 contact info |
NL (GRONINGEN) | hostInstitution | 1˙498˙846.00 |
| 2 |
RIJKSUNIVERSITEIT GRONINGEN
Organization address
address: Broerstraat 5 contact info |
NL (GRONINGEN) | hostInstitution | 1˙498˙846.00 |
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Obiettivo del progetto (Objective)
'Not all cells in bacterial populations exhibit exactly the same phenotype, even though they grow in the same environment and are genetically identical. One of the main driving forces of phenotypic variation is stochasticity, or noise, in gene expression. Possible molecular origins contributing to noise in protein synthesis are stochastic fluctuations in the biochemical reactions of gene expression itself, namely transcription and translation.
The driving hypothesis of this application is that the human pathogen Streptococcus pneumoniae utilizes noisy gene expression to successfully colonize and invade its host. To test this supposition, the total amount of noise in key regulatory networks for virulence factor production will be quantified. Using natural and synthetic bistable switches as highly sensitive probes for noise, in combination with state-of-the-art single-cell imaging, microfluidics and direct transcriptome sequencing, the molecular mechanisms underlying noise generation in S. pneumoniae will be determined. By constructing strains with altered levels of phenotypic variation, the importance of noisy gene expression in S. pneumoniae pathogenesis will be tested.
S. pneumoniae is a leading cause of bacterial pneumoniae, meningitis, and sepsis worldwide. The molecular mechanisms that cause switching of S. pneumoniae to its virulent states are barely understood, although it becomes increasingly clear that noise-driven phenotypic variation plays an important role in pneumococcal pathogenesis. Therefore, understanding the molecular origins of phenotypic variation in S. pneumoniae might not only provide novel fundamental insights in gene expression, but also result in the identification of new anti-pneumococcal targets.'