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© Research
Event

[Canceled] Whole cell model and engineering of Mycoplasma pneumoniae as an universal vaccine

Scientific Fields
Diseases
Organisms
Applications
Technique
Date
20
Apr 2017
Time
14:00:00
Institut Pasteur, Rue du Docteur Roux, Paris, France
Address
Building: Monod (66)
Location
2017-04-20 14:00:00 2017-04-20 15:00:00 Europe/Paris [Canceled] Whole cell model and engineering of Mycoplasma pneumoniae as an universal vaccine Luis Serrano Pubul will talk about Whole cell model and engineering of Mycoplasma pneumoniae as an universal vaccine M. pneumoniae is the causative agent of atypical pneumonia and other extra-pulmonary pathologies in human. Its […] Institut Pasteur, Rue du Docteur Roux, Paris, France Claudia Chica claudia.chica@pasteur.fr

About

Luis Serrano Pubul will talk about Whole cell model and engineering of Mycoplasma pneumoniae as an universal vaccine

M. pneumoniae is the causative agent of atypical pneumonia and other extra-pulmonary pathologies in human. Its small genome size (816 Kbp) and the large repertoire of existing resources about it make this bacterium an ideal model to engineer a therapy chassis. M. pneumoniae has the following advantages: i) It is a mild pathogen that is not life-threatening and can be successfully treated with antibiotics; ii) It has a “simple” metabolic and genetic network, which reduces the risk of unwanted interference of the engineered network. We have quantitative data on the majority of its metabolites as well as a flux-balance model; iii) It does not have cell wall and therefore does not trigger a strong inflammatory response; iv) It has a low rate of recombination with a reduced risk of horizontal transfer to other organisms, as it uses the stop codon UGA to encode for tryptophan; v) Its main antigens and virulence factors have been well characterized; vi) M. pneumoniae can be grown in a defined synthetic serum-free medium (although poorly compared to rich medium); vii) We have also recently sequenced 22 pathogenic strains to determine gene variability and pathogenic genes in the infection process. Comparison of variability with in vitro essentiality identifies possible unknown virulence factors; viii) It is one of the bacteria for which more quantitative and extensive datasets have been obtained. Work from our group has resulted in comprehensive quantitative datasets for its transcriptome, metabolome, proteome, phospho- and lys-acetyl-proteome, and DNA methylome. A comprehensive mini-transposon mutant library obtained by “haystack mutagenesis” has been established, and a full essentiality analysis of all its chromosome elements has been performed (Lluch et al., 2014; submitted). Regarding transcription, we have ChIP-seq data for more than 200 proteins, and we have more than 300 gene-expression perturbation assays that have been analyzed by microarrays, tiling arrays, and deep sequencing. We have a preliminary 3D structure of its chromosome at less than 8000-base resolution, and we are progressing to 1000-base resolution that will allow us to link chromosome structure with transcription regulation. We know the RNA and protein copy numbers, as well as their half-lives; ix) Finally, we have a whole cell model based of the related bacterium M. genitalium that could be used as a basis for constructing a M. pneumoniae model for cell engineering. To develop this whole-cell model, we are producing new targeted data that will be integrated with existing knowledge. In parallel we are developing the tools for generating the non-pathogenic chassis on which we will build antigenic determinants. Here I will discuss the problems associated with building a whole cell model that could be used for engineering, as well as the progress and preliminary data showing the possibilities of using M. pneumoniae as a therapeutic agent.

 

Location

Building: Monod (66)
Address: Institut Pasteur, Rue du Docteur Roux, Paris, France