EMBL Seminars

Abstract
My program develops computational and data science-driven models, deeply grounded in experimental and theoretical biology, to uncover evolutionary and functional relationships between microbes and their ecosystems. We are interested in microbial and viral communities as sensors of ecosystem health, and we work to harness the information contained within microbial communities to monitor and improve human and environmental health. Our recent work using protein language models to decipher viral protein function and expand our ability to see into previously obscured regions of viral sequence space speaks to the power of artificial intelligence (AI) methods to find hidden connections in biology. I will describe applications of this work to understand how phages impact human physiology in disease, and more broadly argue (1) biological AI may require non-standard approaches for data curation, different model architectures, and training protocols that represent the structure and complexity of biological data; (2) the extraordinary sequence diversity of microbial ecosystems enables better AI for biology.   

Connection details
Zoom*: https://embl-org.zoom.us/j/92966299608?pwd=wpPIIaelhRBWO12N1MbaSkBHQ9a7or.1 

Meeting ID: 929 6629 9608 
Passcode: 999646 

Please note that the talk will /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
Developmental plasticity in response to environmental conditions is a characteristic property of organisms that allows for substantial adaptive adjustment at the individual level. Evolutionary biologists have generally accounted for such plasticity by assuming that the individual's responses to its environment are genetically pre-programmed. Studies of transgenerational plasticity in the annual plant Polygonum persicaria provide new insights that challenge this view. Experimental tests of contrasting parental light and soil moisture treatments show that parental and grandparental conditions influence the phenotypes expressed by progeny. Moreover, conditions during the parental generation affect how progeny respond developmentally to their own environments. Individual phenotypes thus reflect a complex developmental integration over time of current and ancestral environmental signals. Because these developmental integration trajectories vary genetically (i.e., as multi-generation Genotype x Environment interactions), the integration process itself can potentially evolve.

We live in an era of unprecedented scientific breakthroughs – gene editing, stem cell research, AI-driven discoveries, and rapid vaccine development are revolutionizing our world. Yet, alongside these advancements, misinformation, ethical dilemmas, and scientific scepticism have become more prominent, raising crucial questions about trust in science.

How do we navigate a "post-truth" society where scientific credibility is constantly challenged? How can researchers, policymakers, and science communicators strengthen the bond between science and society?

The 2025 Science & Society Conference "In Science We Trust?" is your opportunity to tackle these pressing issues head-on. Over two thought-provoking days, we’ll examine how public perception of science has evolved, explore the societal impact of trust in research, and discuss the role of scientists in fostering transparency and engagement. Through inspiring keynote speeches, lively panel discussions, and poster sessions, you’ll gain insights from leading experts and discuss together about the future of trust in science.

The conference welcomes not only life science researchers and students, but also professionals from different fields who are dedicated to fostering a trustworthy relationship between science and society. Whether you are a science communicator, educator, policy-maker, ombudsman or ethicist, this event is sure to be of interest to you!

Abstract
Drastic epigenetic reprogramming occurs during mammalian early embryogenesis. Deciphering the molecular events underlying these processes is crucial for understanding how epigenetic information is transmitted between generations and how life really begins. Probing these questions was previously hindered by the scarce experimental materials that are available in early development. By developing a set of ultra-sensitive chromatin analysis technologies, we investigated chromatin reprogramming during early mouse development for chromatin accessibility, histone modifications, and 3D architecture. These studies unveiled highly dynamic and non-canonical chromatin regulation during maternal-to-zygotic transition and zygotic genome activation (ZGA). However, how ZGA is kickstarted and how the early development program is progressively driven by transcription factors (TFs) remain enigmatic. Recently, we identified key TFs that act at the onset of ZGA, and those that connect ZGA to the first cell fate commitment. In this talk, I will discuss how TFs and epigenetic factors cooperatively establish embryonic program and restore the embryonic epigenomes when the life begins. 

Abstract
Memory formation relies on a bidirectional interplay between synaptic plasticity and nucleus-templated transcriptional programs, but how precisely this interplay is orchestrated by epigenetic mechanisms remains to a large extent unknown. In this talk, I will showcase our recent efforts to better understand this aspect from two angles. First, we have found that chromatin plasticity in the mouse brain is a key determinant for memory allocation, the process by which neurons become recruited into the memory trace: When we increased chromatin plasticity by enzymatic overexpression of histone acetyl transferases (HATs), neurons with elevated histone acetylation were preferentially recruited into the encoding ensemble and memory retention was enhanced, while optogenetic silencing of the epigenetically altered neurons prevented memory expression. Second, we have found that after learning, the epigenetic make-up of a single locus in the encoding ensemble is necessary and sufficient to bidirectionally alter memory performance across different phases of memory consolidation. Together, these findings stipulate that before and after memory encoding, epigenetic mechanisms play a pivotal role as molecular memory aids.