One Health challenge to control vector borne diseases
| Host Institution |
Université Paris-Saclay |
|---|---|
| Start | 2024-11-27 09:15:00 |
| End | 2024-11-27 12:15:00 |
| Duration | 3 hours |
| Mode | Online |
| Location | Universite Paris-Saclay |
| Target Groups | Academic Staff; Administrative Staff; Master students; PhD students; Post-docs; Public; Researchers; Undergraduate students |
| Contact Person | Sébastien Pomel sebastien.pomel@universite-paris-saclay.fr |
“One Health challenge to control vector borne diseases”
In a context of global warming, vector borne diseases are spreading worlwide. In this Conference, the development of new strategies of control of two vector borne diseases, i.e. malaria and leishmaniasis, will be presented from the fundamental knowledge of their biology, and in relation with the One Health concept.
Wednesday 27th November 2024
9:15 am – 12:15 pm
For the students from partner universities this event will be accessible as an online conference (link for connection will be sent later)
On-site only for Université Paris-Saclay' students (Room 2000, HM1)
Université Paris-Saclay - Building Henri Moissan - 17, avenue des Sciences, 91400 Orsay, FRANCE
For the local students (only Université Paris-Saclay students) willing to participate on-site , please kindly confirm your presence by sending an e-mail to the organizer.
sebastien.pomel@universite-paris-saclay.fr
Programme of the event
- 9:15 - 9:30 Welcome words
- 9:30 - 10:15 Dr Markus MEIßNER
(Full Professor, Head of Laboratory, Chair for Experimental Parasitology, Faculty of Veterinary Medicine, Ludwig-Maximillians-Universität MÜNCHEN - GERMANY)
“The chromatin remodeler Snf2L is required for Plasmodium just-in-time gene expression”
- 10:15 - 10:45 Coffee break - Discussions
- 10:45 - 11:30 Dr Joana SANTOS
(CNRS Researcher, Head of the Team MalReg, UMR CNRS 9198, I2BC, Université Paris-Saclay, GIF-SUR-YVETTE - FRANCE)
“Single-cell RNAseq reveals that the malaria parasite prepares for life within the host by activating a transcriptional cascade”
- 11:30 - 12:15 Dr Sébastien POMEL
(Associate Professor, Team Parachem, UMR CNRS 8076, BioCIS, Université Paris-Saclay, ORSAY)
“Host-cell directed therapy: a new strategy for the treatment of leishmaniases”
Prof. Dr Markus Meißner
Markus Meißner studied biology at the University of Regensburg and received his PhD from the Ruprecht-Karls-University Heidelberg in 2002. Between 2002 and 2004, he worked at the Imperial College in London and the Walter and Eliza Hall Institute in Melbourne on a Feodor-Lynen-Fellowship from the Alexander von Humboldt Foundation, Germany. In 2004, Markus Meißner returned to Germany and led a BMBF-funded BioFuture research group at the Center for Infectious Diseases at the University Hospital in Heidelberg. In 2009 he received a Wellcome Trust Senior Fellowship and accepted a position as “Scottish University Life Science Association (SULSA)” readership at the Wellcome Trust Centre for Molecular Parasitology at the University of Glasgow. Thereafter, he received an ERC Starting grant in 2012 and was appointed full Professor. Markus Meißner accepted the position as Chair for Experimental Parasitology at the Faculty of Veterinary Medicine of the Ludwig-Maximilian-University (LMU), Munich in 2017. His research interests focus on unique aspects of apicomplexan cell biology, including mechanisms involved in host cell invasion and egress.
Abstract:
The complex life cycle of the malaria parasite Plasmodium falciparum (Pf) involves several major differentiation stages, each requiring strict control of gene expression. Fundamental changes in chromatin structure and epigenetic modifications during life cycle progression suggest a central role for these mechanisms in regulating the transcriptional program of malaria parasite development. The chromatin remodelers that are critical for shaping chromatin structure are not conserved and are unexplored in Pf. We identify PfSnf2L as an ISWI-related ATPase that actively repositions Pf nucleosomes in vitro. PfSnf2L globally controls just-in-time transcription by spatiotemporally determining nucleosome positioning at the promoters of stage-specific genes. The unique sequence and functional properties of PfSnf2L lead to the identification of an inhibitor that specifically kills P. falciparum and phenocopies the loss of correct gene expression timing. The inhibitor represents a new class of antimalarial transmission-blocking drugs, inhibiting gametocyte formation.
Dr Joana Santos
Joana Santos became interested in parasites when she listened to a seminar by Maria Mota during her bachelor in Biology and Genetics at the University of Lisbon, Portugal. After graduating, she moved to NY, US, where she did a one year internship in the team of Photini Sinnis, at NYU, working on liver infection by the rodent malaria parasite sporozoites. In 2006, she moved to Geneva, Switzerland, to do her PhD in the team of Dominique Soldati, as part of the MalPar Marie Curie training network. There, she worked with the Toxoplasma parasite. In 2011, with the support of SNSF and EMBO postdoctoral fellowships, she moved back to the US to undergo her postdoc in the team of Manuel Llinás, first at Princeton University and afterwards at the Pennsylvania State University. During her postdoc, she became interested in mechanisms of gene regulation in Plasmodium falciparum. In 2017, she moved to France, where she first did a short postdoc in the Khamlichi team at the IPBS in Toulouse and then, in 2020, with the support of an ATIP-Avenir grant, she started her own team at the I2BC, in Gif-sur-Yvette, focusing on transcriptional regulation of the malaria parasite. In 2020 she was also recruited at the CNRS as a permanent researcher.
Abstract:
The intraerythrocytic developmental cycle (IDC) during which the malaria parasite Plasmodium falciparum multiplies asexually within the human host red blood cell is the symptomatic stage of the life cycle. The IDC initiates when parasite stages called merozoites are released into the bloodstream, following schizont rupture, and invade the host red blood cells. The merozoite is the less studied stage of the IDC, despite its importance for the establishment of infection. We did the first transcriptional profiling of merozoites throughout development inside the schizont and after egress. Merozoites within the schizont, activate a series of tightly regulated gene expression programs, each encoding for proteins implicated in a specific process required for invasion and life within the host. After schizont egress, free merozoites still express some of these programs but, upon invasion, cells have a distinct transcriptional profile. Remarkably, apart from the expression programs dedicated to translation, over 50% of the genes expressed by merozoites have no human counterparts, making them interesting from a therapeutic point of view. The gene expression programs are regulated by specific transcription factors and chromatin accessibility as well as post-transcriptional mechanisms. I will show how we can explore gene regulation in the parasite for drug discovery.
Dr Sébastien Pomel
Sébastien Pomel received his PhD in 2005 in the Université of Clermont-Ferrand where he worked on a ciliated protozoa: Paramecium. From 2006 to 2008, he moved to the University of North Carolina, USA, to work as a postdoctoral researcher on a protozoan parasite from the apicomplexan family: Toxoplasma gondii. From 2008 to 2010, he went back to France, in the Institut Pasteur de Lille, where he performed a second postdoc on another apicomplexan parasite: Plasmodium falciparum. He was then recruited as an Assistant Professor in 2010 in the Université Paris-Sud, where he has been working on the development of drugs against several groups of protozoan parasites, especially Leishmania.
Abstract:
Leishmaniases cover a range of diseases caused by the protozoan parasites from the genus Leishmania. Currently, leishmaniasis threatens 1 billion people in more than 90 countries over the world, with up to 1 million new cases and 30,000 deaths occurring annually. Leishmaniases can manifest in three major forms: cutaneous, mucocutaneous and visceral leishmaniasis, the latter being fatal in the absence of treatment. Within mammals, Leishmania is an intracellular parasite that resides in a vacuolar compartment called parasitophorous vacuole (PV) interacting extensively with host-cell trafficking machinery and contributing to its survival and proliferation within the host cell. Conventional antileishmanial chemotherapy includes only few treatments presenting main issues of high cost, toxicity and drug resistance. Considering this latter, conventional drugs have to be managed in the field in a One Health context, and new non-toxic antileishmanial drugs have to be developed, without inducing drug resistance. In this way, an alternative approach consists in the development of compounds indirectly targeting the parasite by interfering with host-cell machinery involved in Leishmania infection. In the present work, the antileishmanial properties of an adamantamine derivative, identified as a drug candidate acting on the parasite via the host cell, will be presented.