How can we best talk to one another about global warming? Climate scientist Kate Marvel, Ph.D. studies the physics of the planet using computational models. But climate change isn't just happening on a computer – it's happening here, in the real world, to us. And even a scientist like Marvel can't help but have feelings about that. Join her as she explores climate science and solutions through the lens of different emotions, from wonder, to anger and fear, and finally to hope. And hear her discuss how we don't need to choose between the hard facts that help us understand climate change and the feelings that help us communicate about it. By embracing both, we gain a fuller picture of what we stand to lose – and all there might be to hope for on a rapidly warming planet.

Book giveaway and refreshments from 6:00–6:25 PM for the first 100 students: Dr. Kate Marvel’s Human Nature: Nine Ways to Feel About Our Changing Planet.

*Refreshments: 7:30-8:30 PM (East Arch Courtyard)

Regulation of Biomolecular Condensates by EWS and the Oncogenic Fusion EWS::FLI1

Food webs are ecological maps that help ecologists describe and understand complex species interactions. Although most species are parasitic, most food webs don’t have parasites. As a result, classic ecological theory has not considered little role for parasites. Whether this matters depends on the roles that parasites play in terms of their biomass density, their effects on hosts, and how they modify predator-prey interactions. On the other hand, although food webs might affect parasite transmission and responses to ecological change, epidemiologists rarely think about disease transmission in a food-web context. Putting parasites and food webs together is technically challenging, but it can give new insights to ecology and disease transmission.

Malaria is transmitted to humans by the infectious bite of female anopheline mosquitoes. We are applying mosquito genome-engineering, human volatilomics and quantitative analyses of mosquito behavior to rank human attractiveness to the African malaria mosquito Anopheles gambiae and elucidate the impact of the malaria parasite Plasmodium falciparum infection on human scent signatures. Dissecting the chemosensory biology of malaria transmission has the potential to reveal novel insights into organismal chemosensation and generate next-generation strategies to combat malaria and other vector-borne diseases.

Yeasts in the subphylum Saccharomycotina provide a powerful system for studying how ecological conditions and evolutionary history shape microbial diversity. My research combines environmental sampling, large-scale genomic resources, and trait data from hundreds of yeast species to understand how these microorganisms interact with their environments and how their metabolic abilities evolve. In this seminar, I will highlight two major themes from my work: uncovering where yeasts, including opportunistic pathogens, exist in natural habitats, and investigating why some yeast species evolve broad metabolic capabilities while others specialize on only a few resources. Together, these approaches reveal how ecological context, metabolic networks, and evolutionary processes contribute to the diversity of yeasts found across environments ranging from soils to animal hosts.

Understanding the mechanisms of speciation and adaptation is a fundamental question in biology that also provides an opportunity to uncover new gene functions of clinical relevance. Highly conserved genetic regulatory pathways shared across diverse vertebrate species have been shaped by adaptive evolution to produce spectacular morphological, behavioral, and ecological diversity. Here I review a decade of my lab’s work investigating the rapid evolutionary transition from generalist algae-eating pupfishes to trophic specialists endemic to hypersaline lakes of San Salvador Island in the Bahamas and Laguna Chichancanab, Mexico. We show that colonizing these niches occurred in stages, beginning with selection on standing genetic variation for feeding behavior, then aided by adaptive introgression from diverse sources, and ending with selection on de novo mutations in key craniofacial genes. We discovered that only 157 single-nucleotide polymorphisms (SNPs) and 87 deletions are fixed between scale-eating and molluscivore specialists despite extensive phenotypic divergence in their craniofacial morphology, metabolism, and behavior. These few differences resulted in major transitions in ecological niches and the colonization of new fitness peaks and novel performance optima for scale-biting. Overall, our work provides a new microevolutionary framework for investigating how major ecological transitions occur in nature and illustrates how both shared and unique genetic variation contributes to diversification and provides a path through complex fitness landscapes for access to novel ecological niches.

Frontotemporal dementia is a devastating degenerative brain disease that causes altered personality, behavior, cognition and often motor impairment. Mutations in the MAPT gene that encodes tau can underlie familial forms of FTD (FTD-tau). Brain organoids from patient-derived induced pluripotent stem cell (iPSC) lines patterned towards the most affected brain region, the cerebral cortex, are valuable human models for understanding disease progression and testing candidate therapeutics. Cerebral cortical organoid modeling is limited by low efficiency, high variability across hPSC donors and lines, and high activation of stress pathways. We developed a novel organoid method and quality control (QC) metrics that enable efficient, scalable production of well-patterned cortical organoids. We validated the protocol by testing on 64 hPSC lines. Well-patterned cortical organoids exhibited markedly lower stress signatures and higher cortical quality scores, similar to those of the developing brain. Applying this protocol across multiple patient donor lines revealed phenotypes associated with the V337M, R406W and IVS10+16 MAPT mutations causing FTD-tau. Notably, approximately a third of primary tauopathy-risk genes identified by GWAS were differentially expressed in progenitor cell populations and newly differentiated neurons. These observations indicate a potential neurodevelopmental contribution to FTD-tau and underscore the value of these models to elucidate disease mechanisms and how the disease evolves over time.