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Novembre 2016

Lundi
07 / 11 / 2016
11h00
"Bacterial conjugation: from molecular dissection to synthetic biology"

 

Fernado de la CRUZ  (Instituto de Biomedicina y biotecnologia de Canatbria (IBBTEC), Spain) 

Invited by the PhD students

 

IBCP Confernce Room level -1

Lundi
14 / 11 / 2016
11h00
"Evolution in Darwin’s Dreamponds: the adaptive radiation of cichlid fishes in East Africa”
 

Walter SALZBURGER  (Univ. Basel)       

 

Salle des Thèses Chantal Rabourdin-Combe

Mardi
15 / 11 / 2016
11h00
"Interfering with mRNA translation as a viralmechanism to evade the immune system and promote cell proliferation"
 

Robin FAHRAEUS (Université Paris Diderot, Hopital Saint Louis, Paris - FRANCE)   

Contact: henri.gruffat@inserm.fr

All Epstein-Barr virus (EBV)-infected cells express the nuclear antigen 1 (EBNA1) but despite the presence of CD8 T cells against EBNA1 epitopes in all virus-carrying individuals, the immune system fails to detect and destroy EBV-expressing cells. In order to achieve this immune evasion, the virus has evolved a mechanism whereby the EBNA1 inhibits its own synthesis in cis in order to suppress the production of antigenic peptides for the major histocompatibility (MHC) class I pathway. Studies on EBNA1-mediated interference with the mRNA translation machinery have revealed novel insights into the source and production of antigenic peptides for the MHC class I pathway. Drug screenings suggest that the unique mechanism whereby EBNA1 controls its own expression is a potential therapeutic target. The other aspect of EBNA1-mediated disruption of ribosomal activity relates to cell proliferation. Burkitt’s lymphomas are characterized by c-myc and EBNA1overexpression but the putative “relationship” between EBNA1 and c-myc in malignant and non-malignant cells still remains relatively unknown. To this adds contradicting reports regarding the oncogenic properties of EBNA1. The first EBNA1 transgenic mice model showed a lymphoma phenotype similar to that seen in eu-myc transgenic animals. Later, a second EBNA1 transgenic mouse was made but with no phenotype. There was no explanation for these discrepancies other than the first model expresses low levels of EBNA1 and the second expresses high levels. We have observed that translation disruption caused by EBNA1 triggers E2F and the induction of c-myc. This stimulates ribosomal biogenesis and it can be speculated that the virus exploits a cellular pathway that senses ribosomal stress and aims to restores ribosomal biogenesis via myc. This can help to explain the different reports on EBNA1’s oncogenic capacity and places EBV together with several other oncogenic viruses that target E2F. However, the mechanism whereby EBV activates E2F indicates a different mechanism as compared to Papilloma or Simian viruses.

Amphi Pasteur CERVI

Lundi
21 / 11 / 2016
10h00
"Organoïd based high content screening"

 

Dr. Xavier GIDROL     

 

 

IBCP Confernce Room level -1                                                                                                            

Lundi
21 / 11 / 2016
11h30
"Structural Biology of the Pneumococcal Surface Proteins: Unraveling  the Pathogenesis and Virulence Mechanisms by  X-Ray Crystallography"

 

Juan A. HERMOSO  (Department of Crystallography and Structural Biology, Spanish National Research Council (CSIC), Madrid, Spain)      

Invited by C. Grangeasse

Juan A. Hermoso is the leader of a research group and Full Professor of the Spanish National Research Council (CSIC) at the Institute of Physical-Chemistry “Rocasolano” in Madrid (Spain). His research focuses on multidisciplinary approach with X-ray crystallography, Protein Engineering and Bioinformatics tools aiming to provide knowledge of the three-dimensional structure of proteins and analysis of their various interactions and ligand complexes as a prerequisite for an in-depth understanding of any biological process. The research interests in his group encompass studies in the mechanisms of virulence and pathogenesis and the means of circumvent them. He focuses on the structural biology of the bacterial surface proteins involved in key functions, such as binding of the pathogen to host cellular receptors, antibiotics resistance, cell division, pathogenesis mechanisms or the remodeling of the peptidoglycan framework, which represent important mechanisms in the process of disease.

IBCP Confernce Room level -1

 
Lundi
21 / 11 / 2016
14h00
"Evolution of Helicobacter and nickel metabolism"
 

Hilde DE REUSE (Institut Pasteur, Département de Microbiologie, Unité Pathogenèse de Helicobacter, ERL CNRS 3526 PARIS - FRANCE)  

Contact: xavier.charpentier@inserm.fr        

Metal acquisition and intracellular trafficking are crucial for all cells and metal ions have been recognized as virulence
determinants in bacterial pathogens. Helicobacter pylori colonizes the acidic stomach of about half of the human population worldwide and is associated with gastric cancer that is responsible for 700,000 deaths every year. Virulence of Helicobacter pylori depends on the metal nickel, cofactor of two enzymes essential for in vivo colonization. In the lab, we are studying the transport, storage and distribution of nickel in H. pylori. I will present the functional characterization of unique nickel-binding proteins of H. pylori that act as nickel stores and are essential for colonization. In addition, I will show our recent identification of a novel nickel transporter that is also required for colonization. Phylogenomics were applied to study the distribution of these proteins in the Helicobacter genus that is divided into two categories, enterohepatic species and gastric species (such as H. pylori) that exclusively colonize the stomach of mammals.
Our data show that during evolution of the Helicobacter genus, acquisition of these proteins by gastric Helicobacter species constituted a decisive evolutionary event to allow Helicobacter to colonize the hostile gastric environment.

Salle des Thèses Chantal Rabourdin-Combe

Mercredi
23 / 11 / 2016
15h00
"A hybrid computational/experimental procedure to improve malaria vaccine design"
 

Cristina FERNANDEZ ARIAS (Rockefeller University, New York - USA)  

Contact: christophe.arpin@inserm.fr

Dr Cristina Fernandez-Arias from the Rockeffer University is a systems immunologist using formal approaches to
investigate immune responses. She is an expert in the anti-malaria vaccination field and will present a computational
framework to improve vaccine design.

 Amphi Pasteur CERVI

Jeudi
24 / 11 / 2016
14h30
"Manipulation of Host phosphoinositide metabolism by Coxiella burnetii : lessons from multiparametric high-content"
 

Matteo BONAZZI (FRE3689 CNRS, Montpellier - FRANCE) 

Contact: thomas.henry@inserm.fr

Matteo Bonazzi is heading a CNRS team termed “Cell Biology of bacterial infections” in Montpellier at the CPBS (Centre d’études d’agents pathogènes et Biotechnologies pour la santé). His team focuses on the obligate intracellular bacterium Coxiella burnetti responsible for the worldwide zoonosis Q fever. Matteo has developed multi-phenotypic screening method to study the cell biology of Coxiella infection and Coxiella virulence factors. He will tell us how Coxellia burnetti manipulates host lipid metabolism to
replicate intracellularly.
Ref: Coxiella burnetii effector CvpB modulates phosphoinositide metabolism for optimal vacuole development.
Martinez E, Allombert J, Cantet F, Lakhani A, Yandrapalli N, Neyret A, Norville IH, Favard C, Muriaux D, Bonazzi M. PNAS. 2016 Jun 7

Salle de Réunion du Sous-sol LR5

 
17-18 /11 / 2016
9h00

International conference

https://lyonsysbio2015.sciencesconf.org/?lang=en

Contact: François Briat   francois.briat@ens-lyon.fr

LyonSysBio is the yearly international conference organized by BioSyL. the Systems Biology Alliance of Lyon (http://www.biosyl.org/).
Our goal is to promote exchanges between scientists from different disciplines (biology, mathematics, computer sciences, physics, social sciences) who are interested in the analysis of the wealth of data generated by modern biology, as well as the construction of the 
necessary modeling tools to gain system level thoughtful insights. In 2016, the conference will be held from November 17th to 18th. Keynote lectures will be delivered by invited speakers, on state-of-the-art advances in various domains of Systems Biology (list available on the conference website). In addition, the conference program leaves ample space for contributed talks and posters for which proposals are welcome. We wish to favor results from truly multidisciplinary works. Please use the online system to submit a one-page abstract (maximum 500 words, in English) by October 10th, 2016: http://lyonsysbio2016.sciencesconf.org To register and to submit an abstract, you will have to create a sciencesconf.org account by filling the on-line registration and submission forms.
Similarly to our previous editions, registration will be free but mandatory for students. Registration fees for non-students will be of 100 euros. A Gala reception will be organized on November 17th.
We are looking forward to welcoming you in Lyon for LyonSysbio 2016! 

 
Vendredi
25 / 11 / 2016
11h00
"Evolution of Primate Testis Transcriptomes”

Mehmet SOMEL (Ankara University)     

 

Salle des Thèses Chantal Rabourdin-Combe

 

 

 

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