User:Jan-willem Veening: Difference between revisions
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=== | ===Research Interests=== | ||
The Veening lab is interested in phenotypic bi-stability in Streptococcus pneumoniae and its importance in virulence of this human pathogen. <br> | |||
We are interested in all aspects of transcriptional regulation, including the study of the bacterial cell cycle.<br> | |||
Streptococcus pneumoniae (the pneumococcus) is a major pathogen causing invasive (pneumonia, meningitis, bacteraemia) and non-invasive (acute otitis media, sinusitis) diseases in young children and in elderly and/or immuno-compromised adults. The last decades have seen the emergence and spread of pneumococcal strains with multiple antibiotic resistance posing a serious threat to human health.<br> | |||
Within genetically identical populations of bacteria, often only specific subpopulations of cells enter the same developmental pathway and exhibit the same phenotype; a phenomenon known as phenotypic bistability or phenotypic heterogeneity. How populations of genetically identical cells bifurcate into phenotypically distinct subpopulations in the same environment is an important question for developmental biology.<br> | |||
It is assumed that phenotypic heterogeneity is generated by bacteria as a bet-hedging strategy to ensure that at least some cells within the clonal lineage prevail under fluctuating stressful conditions. Alternatively, phenotypic heterogeneity can act as a ‘division of labour’ process whereby some cells sacrifice themselves to increase the survival chances of its clonal siblings, generate biofilms or successfully colonize its host. Importantly, these mechanisms are often employed by pathogenic bacteria to elude the host immune response, resist antibiotic pressure or invade the host. Obviously, the understanding of differential bacterial development and how bacteria deal with stress is crucial for the control of pathogens<br> | |||
Within the Veening lab we are interested which molecular mechanism the pneumococcus utilizes to generate phenotypic heterogeneity to aid its survival and proliferation in the host. Using a multidisciplinary approach which includes standard molecular biological techniques, clever genetic screens, DNA-microarrays, Mathematical Modelling, and state of the art single cell techniques such as fluorescence time-lapse microscopy and FACS we try to answer some of these important fundamental questions. <br> | |||
===Publications=== | ===Publications=== | ||
http://www.ncbi.nlm.nih.gov/pubmed?term=veening%20jw | |||
Latest revision as of 07:47, 20 April 2012
Contact Info
Dr. Jan-Willem Veening
Assistant Professor
Molecular Genetics Department
University of Groningen
Nijenborgh 7
Building 5172 room 06.40
9747 AG Groningen
the Netherlands
http://www.molgenrug.nl
j.w.veening@rug.nl
Also see http://www.rug.nl/staff/j.w.veening/index
Research Interests
The Veening lab is interested in phenotypic bi-stability in Streptococcus pneumoniae and its importance in virulence of this human pathogen.
We are interested in all aspects of transcriptional regulation, including the study of the bacterial cell cycle.
Streptococcus pneumoniae (the pneumococcus) is a major pathogen causing invasive (pneumonia, meningitis, bacteraemia) and non-invasive (acute otitis media, sinusitis) diseases in young children and in elderly and/or immuno-compromised adults. The last decades have seen the emergence and spread of pneumococcal strains with multiple antibiotic resistance posing a serious threat to human health.
Within genetically identical populations of bacteria, often only specific subpopulations of cells enter the same developmental pathway and exhibit the same phenotype; a phenomenon known as phenotypic bistability or phenotypic heterogeneity. How populations of genetically identical cells bifurcate into phenotypically distinct subpopulations in the same environment is an important question for developmental biology.
It is assumed that phenotypic heterogeneity is generated by bacteria as a bet-hedging strategy to ensure that at least some cells within the clonal lineage prevail under fluctuating stressful conditions. Alternatively, phenotypic heterogeneity can act as a ‘division of labour’ process whereby some cells sacrifice themselves to increase the survival chances of its clonal siblings, generate biofilms or successfully colonize its host. Importantly, these mechanisms are often employed by pathogenic bacteria to elude the host immune response, resist antibiotic pressure or invade the host. Obviously, the understanding of differential bacterial development and how bacteria deal with stress is crucial for the control of pathogens
Within the Veening lab we are interested which molecular mechanism the pneumococcus utilizes to generate phenotypic heterogeneity to aid its survival and proliferation in the host. Using a multidisciplinary approach which includes standard molecular biological techniques, clever genetic screens, DNA-microarrays, Mathematical Modelling, and state of the art single cell techniques such as fluorescence time-lapse microscopy and FACS we try to answer some of these important fundamental questions.
