| Home | Registration | Program | Location | Flyer |
| 09:00 - 10:00 | Plenary talk: Stochasticity in Biology: a Philosophical Analysis of its Potential Explanatory Role |
| Francesca Merlin | |
| After briefly reviewing the history of the concept of noise in biological research, I will discuss a number of philosophical issues, both conceptual and epistemological, about the way biological noise is invoked and studied. Then, in line with recent theoretical and experimental results, especially in cellular and developmental biology, but not only, I will argue for noise, which I will rather call "stochasticity", as an explanatory concept in biology. In particular, I will address the question of what stochasticity (i.e., chance more generally) can explain in this disciplinary context and how. |
| 10:00 - 10:30 | Coffee break |
| 10:30 - 11:30 | Keynote: From Splicing Noise to Disease: When Errors Matter |
| Maria Carmo-Fonseca | |
| Splicing is inherently noisy, with errors occurring occasionally during splice site recognition. Yet, these errors are normally tolerated in healthy individuals. Genetic variation may enhance splicing noise, without disrupting cellular homeostasis. In my laboratory, we are interested in understanding the interplay between stochastic splicing errors and those driven by genetic variants, focusing on the thresholds that separate benign variability from pathogenic consequences. By dissecting splicing errors linked to genetic variants that are not associated with disease, I will discuss how cells buffer splicing noise and when this tolerance fails, leading to disease phenotypes. Understanding these thresholds may provide key insights into the evolutionary pressures shaping transcriptome resilience and the molecular origins of genetic disorders. |
| 11:30 - 12:00 | TBA |
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| 12:00 - 12:30 | TBA |
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| 12:30 - 14:00 | Lunch |
| 14:00 - 15:00 | ECR flash talks & poster |
| 15:00 - 16:00 | Discussion |
| 16:00 - | Social activity & dinner |
| Stocherkahn boat ride along the Neckar river |
| 09:00 - 10:00 | Keynote: Evolution of Regulatory Networks Controlling Plasticity in Gene Expression between Saccharomyces cerevisiae and Saccharomyces paradoxus |
| Patricia Wittkopp | |
| Organisms often cope with changes in their environments by modifying gene expression levels, which can affect their cellular function. This plasticity in gene expression arises when cells sense a change in their environment and alter the activity or availability of trans-regulatory factors, which interact with each gene’s cis-regulatory sequences to determine its expression. To understand how regulatory networks controlling plasticity in gene expression evolve, we used RNAseq data from the baker’s yeast Saccharomyces cerevisiae, its close relative Saccharomyces paradoxus, and their F1 hybrids collected at multiple time points following the transfer of cells from standard laboratory conditions to four different environments (low phosphorus, low nitrogen, increased temperature, and decreased temperature). We also looked at how gene expression changes throughout the cell cycle and during the transition from log phase to stationary phase. In all six datasets, we compared gene expression levels between S. cerevisiae and S. paradoxus and asked how expression plasticity has diverged. We then tested for divergence in expression plasticity between the two species-specific alleles in F1 hybrids, allowing us to disentangle the effects of divergence in cis- and trans-regulation. We found many cases where expression plasticity had diverged between species, most of which were unique to a single environment and attributable primarily to trans-regulatory divergence. We then investigated potential sources of this trans-regulatory divergence by testing 46 transcription factors for effects on expression plasticity resulting from cells being moved to the low nitrogen environment. We found several cases where deletion of a transcription factor had different effects on a gene's expression plasticity in the two species, implying divergence in the regulatory network controlling environment-specific expression. With prior work identifying such changes for only a few genes between much more distantly related species, this work suggests that connections in regulatory networks are changing more often, and over shorter evolutionary timescales, than previously appreciated. |
| 10:00 - 10:30 | Coffee break |
| 10:30 - 11:00 | TBA |
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| 11:00 - 11:30 | TBA |
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| 11:30 - 12:30 | ECR flash talks & poster |
| 12:30 - 14:00 | Lunch |
| 14:30 - 15:00 | Discussion |
| 15:00 - 16:00 | Keynote: Drift in Individual Behavioral Phenotype as a Strategy for Unpredictable Worlds |
| Benjamin de Bivort | |
| Individuals, even with matched genetics and environment, show substantial phenotypic variability. This variability may be part of a bet-hedging strategy, where populations express a range of phenotypes to ensure survival in unpredictable environments. In addition phenotypic variability between individuals (“bet-hedging”), individuals also show variability in their phenotype across time, even absent external cues. There are few evolutionary theories that explain random shifts in phenotype across an animal's life, which we term drift in individual phenotype. We use individuality in locomotor handedness in Drosophila melanogaster to characterize both bet-hedging and drift. We use a continuous circling assay to show that handedness spontaneously changes over timescales ranging from seconds to the lifespan of a fly. We compare the amount of drift and bet-hedging across a number of different fly strains and show independent strain specific differences in bet-hedging and drift. We show manipulation of serotonin changes the rate of drift, indicating a potential circuit substrate controlling drift. We then develop a theoretical framework for assessing the adaptive value of drift, demonstrating that drift may be adaptive for populations subject to selection pressures that fluctuate on timescales similar to the lifespan of an animal. We apply our model to real world environmental signals and find patterns of fluctuations that favor random drift in behavioral phenotype, suggesting that drift may be adaptive under some real world conditions. These results demonstrate that drift plays a role in driving variability in a population and may serve an adaptive role distinct from population level bet-hedging. |
| 16:00 - 16:30 | Coffee break |
| 16:30 - 17:00 | TBA |
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| 17:00 - 17:30 | TBA |
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| 17:30 - 19:00 | Free time |
| 19:00 - | Dinner |
| 09:00 - 10:00 | ECR flash talks & poster |
| 10:00 - 10:30 | Coffee break |
| 10:30 - 11:30 | Discussion |
| 11:30 - 12:30 | Keynote: The Population Genetics of Biological Noise |
| Daniel Weinreich | |
| Noise is intrinsic to information transmission, and information transmission is intrinsic to life. Critically, while biological noise is random, its amount in any organism is in part genetically determined. Here, we explore the population genetic fate of alleles that heritably influence the amount of biological noise in their carrier. We argue from first principles that biological noise is a double-edged sword: almost always deleterious but also occasionally yielding high fitness phenotypes. We further suggest that this implies the existence of an equilibrium amount of noise, at which the advantage of producing additional, rare beneficial phenotypes is exactly balanced by the cost of producing the vastly more common deleterious phenotypes. We predict that the location of this equilibrium in any species will reflect the rate at which its environment is changing, the heritability of realized noise, the model of selection, and population size. Our framework generalizes modifier theory sensu Altenberg, Feldman and others, and resolves teleological criticisms of the hypothesis that evolvability can evolve. We conclude with an outline of open theoretical and empirical questions posed by this framework. |
| 12:30 - 14:00 | Lunch |
| 14:00 - 14:30 | TBA |
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| 14:30 - 15:00 | TBA |
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| 15:00 - 16:00 | ECR flash talks & poster |
| 16:00 - 16:30 | Coffee break |
| 16:30 - 17:30 | Discussion |
| 17:30 - 19:00 | Final discussion & wrap up |
| 19:00 - | Conference dinner |