September 2017
|
Jeudi 03/10/2019 Amphi Biomérieux Séminaire externe |
« An epitranscriptomic switch defines the cytoplasmic fate of the HIV-1 genomic RNA » | |
|
|
Ricardo SOTO RIFO (Institute of Biomedical Sciences, Universidad de Chile) Contact : Emiliano Ricci The HIV-1 genomic RNA (gRNA) plays two major roles in the cytoplasm of infected cells serving as the mRNA for the synthesis of the structural proteins Gag and Gag-Pol but also as the genome packaged into newly produced viral particles. However, the mechanism allowing the discrimination between these two functions has remained elusive for several years. It was recently reported that the HIV-1 gRNA contains N6-methyladenosine (m6A), which was proposed to play a positive role in viral gene expression. We provide evidence for a negative role of m6A in HIV-1 genomic RNA packaging. As such, we identified two adenosine residues located within the 5´- untranslated region as the key residues involved in this regulation. Interestingly, we observed that the Gag protein associates with the RNA demethylase FTO and drives demethylation of the HIV-1 gRNA to promote packaging. We finally demonstrate that this epitranscrioptmic regulation can be targeted pharmacologically using a specific Inhibitor of the FTO RNA demethylase activity. |
|
|
Vendredi 04/10/2019 Salle des Thèses CRC Séminaire Externe |
« Epigenetics meets mathematics: The fusion of experiment and theory brings insights beyond intuition» | |
|
|
Epigenetic gene regulation is highly stable: epigenetic memory of gene expression states can persist over many cell generations and potentially for longer. However, epigenetic regulation is also flexible: genes that are subject to epigenetic regulation can respond dynamically to environmental and developmental signals. How can epigenetic regulation be both stable and flexible? I propose that the key lies in the highly dynamic nature of epigenetic systems. Over the last two decades it has become clear that the nucleus is an extraordinarily busy and noisy place: many proteins, including epigenetic regulators, are in constant motion, exchanging rapidly between chromatin bound and free states. Quantitative aspects of this motion are highly regulated. I propose that that to fully understand this regulation, epigenetics needs mathematics. We need ‘‘moving models’’ built of mathematical descriptions, which we can feed with measured values of quantities and mobilities of the components. A good model makes testable predictions that tell us whether our hypothesis makes sense. If it does not, we change the model. There has never been a better time to combine theoretical approaches with quantitative experiments. On the theoretical side, the last decade has seen a quiet revolution in the application of models built by physicists to the deep questions of epigenetics. On the experimental side, the advent of technologies that allow real time analysis at the single cell and single molecule level, together with those that enable targeted genome editing, allow precise perturbation and quantitative measurements at an unprecedented level. It is time for epigenetics to meet mathematics. I will give examples from work in the field and in my own lab, of how the fusion of experiment and theory has brought fresh insights into epigenetic regulation that go beyond intuition. | |
|
Jeudi 10/10/2019 Amphi Pasteur Séminaire Externe |
“ Circadian regulation of virus replication ” | |
|
|
Dr. Jane McKEATING (Nuffield Department of Medicine, University of Oxford – UK)
contact : francois-loic.cosset@ens-lyon.fr
All living organisms follow a circadian rhythm that coordinates physiological, behavioural and biochemical responses to the environment. Such daily variations include the risk of infection and it is now well recognised that host innate and adaptive immune responses are circadian regulated and influence susceptibility to infectious agents and response to vaccines. Understanding the selective advantage the circadian clock confers on viral fitness will provide fundamental insights into virus-host cell interactions. |
|
|
Vendredi 11/10/2019 11H00 Amphi Pasteur Séminaire Externe |
“ Metabolic control of monocyte and macrophage functions ” | |
|
|
Dr Stoyan IVANOV (U1065 ; Université de Nice) Contact : sulliman.omarjee@ens-lyon.fr
Monocyte and macrophage diversity is evidenced by the modulation of cell surface markers and differential production of soluble mediators. These immune cells play key roles in controlling tissue homeostasis, infections, and excessive inflammation. Recently, it became clear that metabolism controls macrophage and monocyte main functions. Modulation of glucose, fatty acid, and amino acid metabolism is associated with various macrophage activations in response to external stimuli. Modulation of environmental factors impacts on immune cell numbers and functions. Warm ambient temperature is atheroprotective and thermoneutrality associates with reduced monocyte egress from the bone marrow in mice and likewise may also suppress blood monocyte counts in man. |
|
|
Lundi 14/10/2019 11H00 Salle Condorcet Séminaire externe |
« Control of cell division orientation during early vascular development » | |
 |
Bert De RYBEL (VIB Ghent, Belgium)
Host: Teva Vernoux
|
|
|
Lundi 21/10/2019 11h Salle Condorcet Séminaire externe |
« Timing under the light of sun and moon » | |
|
|
Kristin TESSMAR ( Max Perutz Labs,Vienna) Host: Michalis Averof |
|
|
Mercredi 23/10/2019 11h Salle Condorcet Séminaire externe |
“ Stop codon readthrough : from basic research to therapeutic application ” | |
 |
Dr Olivier NAMY (Institut de Biologie Intégrative de la Cellule CNRS UMR9198 - Orsay)
Contact : laurent.chavatte@ens-lyon.fr
Nonsense mutations, generating premature termination codons account for 10% to 30% of the mutations found in human genetic diseases. Nonsense translational suppression, induced by small molecules including gentamicin and G418, has been suggested as a potential therapy to counteract the deleterious effects of nonsense mutations in several genetic diseases and cancers.
This therapeutic approach is currently limited by the small number of available drugs promoting stop codon readthrough and by our lack of knowledge about tRNAs that are able to decode stop codons. We performed an HTS of >17000 compounds to identify new readthrough inducers. In parallel we addressed the role of modifications found in the anticodon loop of several tRNAs on their ability to recognize the stop codon. We show that almost systematically, the modification confers to these tRNAs the ability to act as a near cognate tRNAs on stop codons, without noticeable impact on their ability to decode cognate or near-cognate sense codons. These findings reveal an important role of modifications for tRNA decoding. |
|
|
Jeudi 24/10/2019 11H00 Amphi Pasteur Séminaire externe
|
“ titre à venir ” | |
|
|
Dr. Thomas HÖFER (DKFZ Heidelberg)
Contact : marlene.dreux@ens-lyon.fr
|
|
|
Lundi 28/10/2019 11h Salle des Thèses CRC Séminaire externe |
« S-acylation – greasing plant protein function » | |
|
|
Piers HEMSLEY (University of Dundee,UK)
Host: Yvon Jaillais
|
|