Hugo Reyes-Centeno HEVA (Human Evolution & Virtual Anthropology Lab) EduceLab

Dr. Hugo Reyes-Centeno is an evolutionary anthropologist specializing on the emergence of modern human anatomy and behavior over the last million years. In addition, he conducts inter-disciplinary research on human biocultural diversity and the study of natural and cultural heritage worldwide. Prior to joining the University of Kentucky in 2020 as Assistant Professor of Anthropology, he served as Scientific Coordinator and co-founder of the Center for Advanced Studies “Words, Bones, Genes, Tools” at the University of Tübingen (Germany), where he also completed a dissertation in the Institute of Archaeological Science and the Senckenberg Centre for Human Evolution and Paleoenvironments. His research has appeared in Cell, PNAS, Journal of Human Evolution, and PLoS Genetics, among other venues. He has performed paleontological and archaeological fieldwork in France, Italy, Peru, the Philippines, and Spain. Currently, he serves as Co-PI of the NSF-funded EduceLab: Infrastructure for Next Generation Heritage Science.

Abstract: Despite consensus on the emergence of anatomically modern humans in Africa and their subsequent dispersal into the rest of the world, the mode and timing of these processes remain controversial topics. In addressing them, data on human anatomical and genomic variation have sometimes generated conflicting inferences. Therefore, approaches that consider both lines of evidence under a common theoretical framework are important for reconciling competing evolutionary models. In this talk, I highlight research that tests competing models of human dispersal out of Africa, which applies quantitative genetic and population genetic methods to anatomical and genomic data. I discuss the caveats of these conclusions, including the influence of admixture between modern humans and other hominins. Furthermore, I examine how these findings align with the known human fossil record and a growing inventory of ancient genomes from archaeological and paleontological contexts. Finally, I review how ongoing field and laboratory projects in Eastern Africa, Southeast Asia, and South America shed light on human evolution, adaptations, and dispersals.

Nicholas Teets

Insect species distributions are tightly linked to winter conditions. Surviving winter requires adaptations to cope with low temperatures and limited food resources, and much of our lab’s work focuses on the underlying mechanisms used by insects to survive extreme winter conditions. In this talk, I will primarily discuss our recent work on survival mechanisms of the Antarctic midge, which is the world’s southernmost insect and the only species endemic to Antarctica. This species can survive freezing of its body fluids for up to nine months a year, but it must also cope with considerable spatial and temporal variability in Antarctica’s unpredictable environments. Here, I will summarize how this impressive beast survives internal freezing, as well as the consequences of microhabitat variability and winter climate warming.

Larvae (left) and adults (right) of the Antarctic midge

Fieldwork

 Erin Dolan

Abstract: A graduate student’s relationship with their research advisor is considered to be the single-most influential factor in the quality and outcomes of their graduate training experience. Indeed, effective mentorship by research advisors promotes the development and success of graduate mentees. Yet, mentoring relationships, like any prolonged relationship, can have negative elements. Little research has examined the problematic elements of graduate research mentoring, even though prior research on mentoring in workplace settings suggests that negative mentoring experiences are common. This seminar will present findings from research on the negative mentoring that graduate life science researchers experience, including how their experiences differ from negative mentoring experienced in workplace settings. The session will offer insights on how mentor behaviors may be experienced as harmful or unhelpful and on how mentees and mentors can identify, avoid, and mitigate the impacts of negative mentoring.

Evangeline Ballerini Ballerini Lab

Evangeline Ballerini is an Assistant Professor in Biological Sciences at California State University, Sacramento. Evangeline’s research examines the evolutionary genetics and developmental biology of traits influencing ecological interactions between plants and pollinators with a focus on the genus Aquilegia. Evangeline earned a BA from the Integrative Biology department at the University of California, Berkeley and a PhD from the Organismic and Evolutionary Biology department at Harvard University and conducted postdoctoral research at the University of Georgia and the University of California, Santa Barbara.

Abstract: The genus Aquilegia, commonly known as columbine, represents a classic example of adaptive radiation following the evolution of a key innovation - floral nectar spurs. Nectar spurs, tubular outgrowths of floral tissue that produce and store nectar, are hypothesized to promote speciation through pollinator specialization. Variation in spur morphology, along with other floral features such as color and orientation, allows flowers to adapt to different animal pollinators, contributing to reproductive isolation. I will present work focused on understanding the genetic basis of trait evolution in the genus Aquilegia at multiple evolutionary timescales. To shed light on how nectar spurs evolved in the Aquilegia ancestral lineage, I will highlight studies in which I used a combination of genomic and transcriptomic analyses to identify a key gene regulating nectar spur development. Focusing on more recent evolutionary history, I will discuss work in which I use similar techniques to explore the genetic basis of several floral traits distinguishing closely related Aquilegia species adapted to different animal pollinators and examine the population genetic processes influencing the evolution of these traits important for ecological speciation in the genus.

Dr. Michael Long

Michael Long is the Thomas and Susanne Murphy Professor of Neuroscience at the NYU School of Medicine. He completed his graduate studies with Barry Connors at Brown University where he investigated the role of electrical synapses in the mammalian brain. During his postdoctoral work with Michale Fee at MIT, Long began to study the songbird model system to uncover the cellular and network properties that give rise to learned vocal sequences. Since beginning his laboratory in 2010, Long has focused his attention on the neural circuits underlying skilled movements, often in the service of vocal interactions. To accomplish this, the Long lab has taken a comparative approach, examining relevant mechanisms in the songbird, a newly characterized neotropical rodent, and humans. In addition to federal funding, the Long lab has also received support from NYSCF, the Rita Allen Foundation, the Klingenstein Foundation, and the Herschel-Weill Foundation.

Long Lab

Abstract:  Vocal communication is central to our everyday lives, facilitating social exchange. Despite significant recent discoveries, the neural mechanisms underlying coordinated vocal exchanges remain poorly understood. We examine the brain processes involved in interactive vocal behaviors, focusing on forebrain circuitry in the songbird and the rodent, and we relate these to emerging human studies that employ a range of methods to manipulate and monitor cortical areas relevant for speech.

Carla Rothlin Rothlin Ghosh Lab

Abstract: Cell death is an invariant feature throughout our lifespan, starting with extensive scheduled cell death during morphogenesis and continuing with death under homeostasis in adult tissues. Additionally, cells become victims of accidental, unscheduled death following injury and infection. Cell death in each of these occasions triggers specific and specialized responses in the living cells that surround them or are attracted to the dying/dead cells. These responses sculpt tissues during morphogenesis, replenish lost cells in homeostasis to maintain tissue/system function, and repair damaged tissues after injury. Wherein lies the information that sets in motion the cascade of effector responses culminating in remodeling, renewal or repair? I will attempt to provide a framework for thinking about cell death in terms of the specific effector responses that accompanies various modalities of cell death. I will discuss an integrated three-fold “cell death code” consisting of information intrinsic to the dying/dead cell, the surroundings of the dying cell and the identity of the responder. I will propose that this can provide a foundation for the prediction of resolving and non-resolving inflammation.