EMBL Seminars

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.

Abstract
In vertebrates, gonadal steroid hormones are the principal drivers of sex-variable biology. As stated in the classical Organizational-Activational Hypothesis, developmental pulses of hormones in early life direct brain sexual differentiation, while sex differences in neurophysiology and behavior emerge with the onset of puberty. Crucially, the gonadal hormones: estrogens, progestins, and testosterone, act primarily through their cognate nuclear receptors, which directly bind DNA to regulate gene expression. Therefore, identifying the gene programs regulated by hormones in distinct neuronal cell types, and at different life stages, is paramount to understanding sex differences in brain function. To this end, my lab discovered the neural target genes of estrogen receptor ERα, which is the master regulator of brain sexual differentiation in rodents. We investigated the relationship between ERα genomic occupancy and sex-biased gene expression in the posterior bed nucleus of the stria terminalis (BNSTp), a sexually dimorphic node in limbic circuitry that modulates sex-differential social behaviors such as mating. In adult animals we observe that levels of ERα are predictive of the extent of sex-variable gene expression, and that these sex differences are a dynamic readout of acute hormonal state. Through analysis of chromatin accessibility across puberty, we find that adult sex differences are driven principally by testosterone, which both opens and closes chromatin in males. In contrast, accessibility of female-biased loci is maintained following gonadectomy, indicating that ovarian hormones do not drive BNSTp sex differences. In neonates we find that transient ERα recruitment at birth leads to sustained chromatin opening and male-biased gene expression, which varies markedly across BNSTp cell types. Our findings demonstrate the exquisite specificity of hormone receptor actions within the brain. We are now investigating the plasticity of sex-variable gene expression across the lifespan, and the consequent effects on neuronal health and disease risk.

Abstract
Complex networks of transcription factors (TFs) allow bacteria to adapt to their environment through (i) the sensing of molecular signals, and (ii) corresponding gene expression responses. Despite decades of work, our current knowledge covers on average less than 10% of TFs regulatory functions and sensed signals in well-studied bacterial species, which falls below 1% in most other species. To address this lack of knowledge, we develop sequencing-based approaches to accelerate the mapping of transcriptional regulatory networks, with recent proof-of-concepts applications on Escherichia coli. As a main tool, we rely on high-throughput protein expression and in vitro DNA-binding assays to identify and characterize TFs interactions with signal molecules and with DNA in a genome-wide manner for up to hundreds of TFs at a time. This work paves the way towards routine near-complete mapping of transcriptional regulatory networks in bacteria.

Connection details
Zoom*: https://embl-org.zoom.us/j/97121685267?pwd=bJilqT0QoXIinBFFqW7reaOwaMDcrR.1

Meeting ID: 971 2168 5267
Passcode: 354388

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.

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. 

Abstract
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Connection details
Zoom*: [https://embl-org.zoom.us/j/96374261689?pwd=TnNxRWtQY2lyc2pSa2JpY3NGcDlhZz09] (Meeting ID: [963 7426 1689], Password: [DBU])

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.