EMBL Seminars

About the speaker
Thomas Hartung is a toxicologist and pharmacologist who is working at the forefront of developing new approach methodologies (NAMs) for toxicology testing. He is the current director of the Centers for Alternatives to Animal Testing (CAAT) in the US and in Europe based at John Hopkins and the University of Konstanz respectively. His group has an interest in AI, neurotoxity, genetics and metabolomics. Before moving to the US, Prof Hartung led the European Center for the Validation of Alternative Methods, working towards the 3 'Rs' - to reduce, refine and replace animal models in toxicology testing. Prof Hartung was a co-organiser of the Exposome Moonshot Project and is part of the organising committee of the Global Exposome Forum.

Meet the speaker
An informal Q & A discussion session will be held after the talk on the same zoom link below. We especially encourage predocs and postdocs to take advantage of this opportunity.

Connection details
Zoom*: https://embl-org.zoom.us/j/92081163221?pwd=ysQ9LwJ4zs6ivM9sr1hBr4xrtYbbY8.1&jst=2 (Meeting ID: 920 8116 3221, Password: 292277)

*For the FAQ section, as a zoom participant, please use either the chat function (the host will read out your question) or the “raise your hand” function and turn on your microphone.

Don’t miss the next Project Management Network event with Tuba Bilecik Antonelos, an international conflict management professional and former corporate attorney with extensive experience in international dispute resolution. For more than two decades, Tuba has helped organizations navigate conflict through negotiation, collaborative problem-solving, and the facilitation of difficult conversations, while strengthening conflict resolution skills at all levels.

Tuba will be delivering a session on “Conflict Resolution for Project Managers”. She will guide participants through understanding their primary conflict style, learning how to flex it in challenging conversations, and building the capacity to handle disagreements more constructively. This session is ideal for project managers, team leaders, and professionals who navigate complex stakeholder relationships and want practical tools to manage and resolve conflict effectively.

In the meantime, if you have any questions, please contact Anna Rupaningal (alr@ebi.ac.uk) or Simone Vegh (vegh@ebi.ac.uk).

Connection details
Zoom*: https://embl-org.zoom.us/j/91320490934?pwd=byBiSfuRTrCLYrrXMoZHOq4k5sqIi1.1&jst=2 (Meeting ID: [91320490934], Password: [759051])

Please note that the talk will be recorded.
*For the FAQ section, as a zoom participant, please use either the chat function (the host will read out your question) or the “raise your hand” function and turn on your microphone.

Antimicrobial resistance is a major global health threat, yet no antibiotics with a novel mode of action have been approved in the last 20 years. While machine learning (ML) accelerates drug discovery by optimizing molecules in known chemical spaces, it struggles to explore novel spaces where new mechanisms of action might exist. We use Generative flow networks (GFlowNets), a novel ML architecture, to sample chemical space in proportion to a reward function (e.g., predicted antibiotic activity). In this way, compounds with low antibiotic activity, which are discarded as inactive in traditional screening, still provide information that can point in the direction of new antibiotic activity peaks. This approach uncovers pathways to molecules with novel activity. To enhance training, we employ bacterial cell painting, which uses fluorescent dyes to generate detailed phenotypic profiles of compound effects at high throughput. By linking these microscopy profiles to known antibiotics and whole genome CRISPRi depletion data, ML models can infer mechanisms of action. Using high-throughput microscopy screening and iterative active learning loops, we aim to identify and validate new antibiotic candidates in unexplored chemical spaces.

See bio here : https://brunlab.com/about-us/people/yves-brun/  

Abstract
African Trypanosomes proliferate within the bloodstream and tissue spaces of mammals and can maintain a long-term infection often lasting for years. To do this, trypanosomes must avoid the host adaptive and innate immune response at the same time as acquiring nutrients from the host. There is a good understanding of how the adaptive immune response is distracted through a population survival strategy based on antigenic variation a densely packed surface coat made of a variant surface glycoprotein (VSG). There is also a strong selection pressure to prolong the survival of individual trypanosomes presumably to increase the chances of returning to a tsetse fly, the definitive host. There is rapid clearance of antibodies bound to the cell surface and a set of conserved receptors that decrease the effectiveness of complement pathways. A second set of receptors is involved in the acquisition of host macromolecular nutrients. 

Why do these conserved receptors not lead to immune clearance?  Work on how the receptors bind ligands, how trypanosomes have evolved to have a wide host range, and what happens when on ligand binding have been integrated to form a model of how they are able to form life-long infections. 

Connection details
Zoom*: https://embl-org.zoom.us/j/99010203982?pwd=eKlBm1821yrpjddaCbanN6CjooJL8y.1 

(Meeting ID: 990 1020 3982, Password: 717935)

Please note that the talk will be recorded.
*For the FAQ section, as a zoom participant, please use either the chat function (the host will read out your question) or the “raise your hand” function and turn on your microphone.

Abstract
Bridging the concentration gap between the dispersed state of intrinsically disordered biopolymers and their high-concentration states relevant for cellular environment, including membrane-less organelles, as well as for food biochemistry and food technology, is a serious challenge. In this talk, I will present an approach based on the conventional and newly developed pulse EPR techniques and aimed to describe the spatial and conformational distributions in biomolecular condensates and weak aggregates. This methodology can potentially also shed light on the biomolecules’ solvation. Furthermore, comparison of pulse EPR data with small angle scattering and THz calorimetry data might appear very interesting. Importantly, new EPR method to determine local biopolymer density will be presented, which might appear an efficient support for SAXS/SANS based determination of conformational ensembles of intrinsically disordered biomolecules.

About the speaker
[Biographical information about the speaker].

Meet the speaker
To meet with the speaker informally after the talks,sign up here [add link]. We especially encourage predocs and postdocs to take advantage of this opportunity.

Attachments
[Link to a file (for example a pdf of the seminar’s programme) - the file can be uploaded on the intranet]

Connection details
Zoom*: [link] (Meeting ID: [XXXXXXXXX], Password: [XXXXXXX])

Please note that the talk will yes/not be recorded.
*For the FAQ section, as a zoom participant, please use either the chat function (the host will read out your question) or the “raise your hand” function and turn on your microphone.

Abstract

Epigenetic components regulate many biological phenomena during development and normal physiology. When dysregulated, epigenetic components can also accompany or drive diseases. One main class of epigenetic components are Polycomb group proteins. Originally, Polycomb proteins were shown to silence gene expression. We found that this function involves the regulation of 3D chromosome folding and we found that Polycomb components can induce the formation of long-distance interactions or chromatin loops that may play instructive roles in gene regulation as well as serve as scaffolding elements that contribute to enhancer-promoter specificity. Perturbation of Polycomb components is involved in human cancer and leads to tumorigenesis in flies. Surprisingly, even upon a transient depletion followed by restoration of the full Polycomb compendium, epithelial cells lose their normal differentiated fate, continue proliferating and establish aggressive tumors, demonstrating that cancer can have a fully epigenetic origin. Similarly, transient perturbation of histone acetylation in mouse ES cells and gastruloids shows that they can record chromatin changes and that this results in cellular memory of the perturbation states. The implication of these data will be discussed.