Click here for more information on Dr. Joseph Takahashi.

Dr. Ricardo Mallarino | Mallarino Lab

Bio:
Ricardo Mallarino is an Assistant Professor of Molecular Biology at Princeton University. Originally from Bogota, Colombia, he graduated with a B.S. in Biology from Universidad de los Andes. He completed his graduate studies at Harvard in Organismic and Evolutionary Biology in 2011, working with Arhat Abzhanov on developmental mechanisms underlying beak shape diversity in Darwin’s finches and their close relatives. After completing his PhD. he joined Hopi Hoekstra’s lab at Harvard, where he established a new model species and developed tools for studying the molecular basis of pigment pattern formation in mammals. Research in the Mallarino lab focuses on understanding the genetic and developmental mechanisms by which form and structure are regulated during vertebrate embryogenesis and elucidating how these processes get modified during evolutionary time to produce phenotypic diversity.

Abstract:
The evolution of metazoan organisms over millions of years has led to remarkable complexity of form and function. While biologists have long studied the ultimate causes of biological diversity (i.e., why it originates), the proximate mechanisms underlying its emergence (i.e., how it arises) remain largely unknown. The goal of my lab is to uncover the genetic and developmental mechanisms underlying the establishment of phenotypic traits and to understand how these mechanisms have evolved to generate diversity across species. We achieve this by harnessing naturally evolved phenotypic variation in ‘non-traditional’ species and integrating multiple disciplines, including developmental biology, computational biology, and evolutionary genetics. For the past six years, our research has focused primarily on patterning and evolution of novelty in mammalian skin. In this talk, I’ll describe how my lab has developed new model systems to study two distinct spatially patterned phenomena during skin development - stripe pattern formation in rodents and gliding membrane formation in marsupials. Through the use of experimental embryology, transcriptomics, comparative genomics, and functional genetics, our work has yielded insights into the mechanisms by which phenotypic novelty is generated at the molecular level.

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Dr. Tiago Simões | Simões Lab

Bio:
Dr. Tiago Simões started his career in his home city (Rio de Janeiro, Brazil), where he obtained his BSc and MSc in Biological Sciences- Zoology at the Federal University of Rio de Janeiro and the National Museum of Brazil. He obtained his PhD at the University of Alberta, Canada, in 2018 working with Dr. Michael Caldwell. Between 2019 and 2023 he was a Postdoctoral Fellow at the Museum of Comparative Zoology & Dpt. Organismic and Evolutionary Biology, Harvard University, working with Dr. Stephanie Pierce, and since 2022 a Research Associate in the Division of Vertebrate Zoology at the American Museum of Natural History. Since 2024, he has been an Assistant Professor in the Dpt. Ecology and Evolutionary Biology at Princeton University.

Dr. Simões’s research integrates data from living and extinct species, as well as morphological and genomic data, to investigate deep time problems in vertebrate evolution, with a special focus on the origin and early evolution of lizards and snakes. He has created several new morphological and total-evidence datasets employing state-of-the-art techniques in Bayesian phylogenetics and phylodynamics that helped bridging gaps between morphological and molecular hypothesis of reptile evolution. These studies, along with new technical advances in phylogenetics have been published in several peer-reviewed scientific articles creating, including in Nature, Nature Ecology & Evolution, and Science Advances. 

:
The history of life on Earth is marked by complex interactions between species genomes and phenotypes across constantly changing environments. Therefore, it is necessary to investigate these interactions across deep evolutionary time to understand the processes responsible for the construction of both past and modern biological diversity. However, this line of research has historically faced several logistic and methodological limitations, such as the lack of quantitative methods for combining various data types sampled across vastly different organismal and temporal dimensions. Fortunately, the past decade has been testimony to several advances in Bayesian evolutionary analyses that have fostered the integration of data types towards more sophisticated inferences of evolutionary trees and macroevolutionary dynamics. Here, I will illustrate how I have used and expanded this class of techniques to integrate molecular and phenotypic data from living and fossil species to understand the patterns and processes operating across major evolutionary transitions in vertebrates, with a special focus on reptiles. These results have overhauled the structure of key areas of the reptile tree of life, including the origin of lizards and turtles, the interplay between phenotypic and molecular innovations during evolutionary transitions, and how these events have been impacted by climate change across deep time. I conclude by highlighting how a new omics era, integrating whole genomes and phenomes, can conciliate historical challenges in understanding organismal evolution and the interplay between genomes and phenotypes with their surrounding environments across broad taxonomic and time scales.

Watch the seminar here!

Dr. Joseph Takahashi | Takahashi Lab

Bio:
Joseph S. Takahashi is the Loyd B. Sands Distinguished Chair in Neuroscience, Investigator Emeritus in the Howard Hughes Medical Institute, and Chair of the Department of Neuroscience at the University of Texas Southwestern Medical Center in Dallas. He joined UT Southwestern in 2009. Takahashi was born in Tokyo, Japan (US Citizen) and grew up in Burma, Italy and the Maryland suburbs of Washington, DC. He graduated from Swarthmore College, Pennsylvania, with a BA in Biology; did his graduate studies with Michael Menaker at UT Austin and University of Oregon, Eugene (PhD in 1981). He was a Pharmacology Research Associate at the NIMH and joined the faculty of Northwestern University in 1983, where he was the Walter and Mary Elizabeth Glass Professor in the Life Sciences at Northwestern University. During his 26-year tenure at Northwestern, he held appointments as professor in the Department of Neurobiology on the Evanston campus and director of the Center for Functional Genomics.

His research interests are the molecular mechanism of circadian clocks, the genetic basis of behavior, and the role of circadian clocks in regulating metabolism, aging and longevity. Dr. Takahashi pioneered the use of forward genetics in the mouse as a tool for discovery of genes underlying neurobiology and behavior, and his discovery of the mouse and human Clock genes led to a description of a conserved circadian clock mechanism in animals. He has gone on to demonstrate critical physiological roles of the clock in metabolism, genome-wide gene expression and epigenetics. Recently he has discovered key roles for circadian clocks in parasitic diseases such as sleeping sickness and malaria. In the field of aging, his lab has recently shown that circadian alignment of feeding under caloric restriction is a major factor in lifespan extension in mice. He is the author of more than 340 scientific publications and the recipient of many awards including the Honma International Prize in Biological Rhythms Research in 1986, W. Alden Spencer Award in Neuroscience from Columbia University in 2001, Eduard Buchner Prize from German Society for Biochemistry and Molecular Biology in 2003, Outstanding Scientific Achievement Award from the Sleep Research Society in 2012, and the Gruber Neuroscience Prize from the Gruber Foundation and the Society for Neuroscience in 2019 (the top award in the field of neuroscience in the USA). He was selected as a Thomson Reuters Highly Cited Researcher in Biology and Biochemistry in 2014 and 2019, and Web of Science Highly Cited Researcher in 2019-2021. He was elected a Fellow of the American Academy of Arts and Sciences in 2000, a Member of the National Academy of Sciences in 2003, and a Member of the National Academy of Medicine in 2014. 

Takahashi has served on a number of advisory committees for the National Institutes of Health, as well as scientific advisory boards for Eli Lilly and Company, the Genomics Research Institute for the Novartis Foundation, The Klingenstein Fund, the Searle Scholars Foundation, the McKnight Foundation, the Allen Institute for Brain Science, the Max Planck Institute for Biophysical Chemistry, the Bristol-Myers Squibb Neuroscience Award Selection Committee, INSPIRE Servier International, and the Restless Legs Syndrome Foundation. He is/was a member of the editorial boards for PNAS, eLife, PLoS Genetics, Neuron, Aging Cell, Curr Opin Neurobiol, Physiological Genomics, J. Biol. Rhythms, Genes Brain Behav, and the Faculty of 1000.  He was also a co-founder of Hypnion, Inc., a biotech discovery company in Worcester, Mass., that investigated sleep/wake neurobiology and pharmaceuticals (now owned by Eli Lilly and Co.), and was a co-founder of Reset Therapeutics, Inc., a biotech company that worked on the role of clocks in metabolism. He is a co-founder of Synchronicity Pharma, a biotech company working on the role of circadian clocks in sleep disorders and cancer.

Abstract:
Genetic analysis of circadian behavior in mice has revealed that the molecular basis of circadian clocks involves an autoregulatory transcriptional network that oscillates with a 24-hour periodicity. In mammals, the discovery of “clock genes” led to the realization that circadian clocks are cell autonomous and are expressed in the majority of cells and tissues in the body. The master circadian pacemaker located in the hypothalamic suprachiasmatic nucleus sits at the top of a hierarchy of oscillators in the body, but peripheral oscillators can and do respond to more proximal signals such as nutrients and metabolites. Thus, the “circadian system” in mammals is a multi-oscillatory hierarchy. In addition to controlling the timing of behavior and physiology, the circadian clock gene network interacts directly with many other pathways in the cell. These include metabolism, immune function, cardiovascular function, cell growth, as well as, the majority of the “hallmarks of aging” pathways. With respect to metabolism, the timing of nutrient consumption is critical, and we and others have shown that restricting the timing of feeding has many health benefits. We have found that time restriction and circadian alignment of feeding are critical factors for extension of lifespan under caloric restriction. Because the circadian gene network is a conserved regulator of aging and longevity in mice and humans and because circadian transcriptional drive declines with age, we are testing interventions that rescue circadian amplitude as agents to promote healthspan and lifespan. We propose that the circadian gene network is a novel target for aging and longevity.

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Dr. Susana Magallón Puebla

Bio:
Dr. Susana Magallón Puebla is the Director of the Biology Institute at the Universad Nacional Autónoma de México. She is an evolutionary biologist who focuses on understanding macroevolutionary processes associated to the evolution of flowering plants, including their floral structure, the timing and dynamics of their diversification, and the mechanisms of acquisition of species richness in diverse Mesoamerican lineages. She obtained her B.Sc. and M.SC. degrees from UNAM, and a Ph.D. from the University of Chicago. She held a postdoctoral fellowship at the University of California, Davis. Her research is characterized by a deep understanding and integration of paleobiology and of phylogenetic comparative methods, involving the combination of morphological and molecular data from extant and fossil species. Dr. Magallón was inducted as a member of the National Academy of Sciences (USA)  and the Royal Society (UK) in 2024 because of the quality of her research and contributions to the scientific community.

Abstract:
Integration of molecular data, to provide a general phylogenetic framework, and morphological data, to allow incorporation of fossils, represents a cardinal approach to investigate evolution in deep time. We assembled a morphological matrix for 1201 extant species representing all angiosperm families, and 121 well-preserved fossil flowers, and in combination with a molecular database for extant species based on exemplar representation, used it to investigate methodological issues relating to integration of extant and fossil taxa in phylogenetic estimation; divergence time estimation in a full Total Evidence approach; and estimation of the theoretical floral morphospace. Phylogenetic analyses used different optimization criteria and kinds of data to estimate relationships, as well as uncertainty in fossil placements. We found that the joint use of molecular and morphological data in a parametric context allows to recover a phylogenetic framework in agreement with molecular estimates, and fossils associated to branches in agreement with assessments based on detailed morphological comparisons. Nevertheless, uncertainty associated to fossil placements is usually high. An attempt to estimate divergence times using morphological, molecular and temporal information indicates that, while available models to integrate extant and fossil species in the same diversification process represent significant advances, there are practical difficulties with fossils for which few characters can be scored, and in the free estimation of model parameters. The theoretical morphospace of floral structure was estimated through the construction of a pairwise distance matrix among extant and fossil species, estimation of disparity, and ordination techniques to reduce dimensionality. The area of the theoretical morphospace occupied by extant and fossil species was identified, as well as how morphospace occupation has changed through time and among groups. A decrease in morphospace occupation towards the present and canalization in the of morphospace occupation among derived clades are documented, in agreement with previous independent observations.


How did the first flower in the history of Earth look like?

Dr. Celina Juliano | Juliano Lab

Bio:
Dr. Juliano joined the faculty at UC Davis in 2015 as an Assistant Professor in the Molecular and Cellular Biology Department and was promoted to Associate Professor with tenure in 2021. She is a developmental biologist with a long-standing interest in stem cell biology. Her doctoral research, mentored by Dr. Gary Wessel at Brown University, focused on understanding the molecular mechanisms underlying the maintenance of plasticity during sea urchin development. Dr. Juliano completed her post-doctoral work at Yale University in the laboratory of Dr. Haifan Lin with co-mentoring from Dr. Rob Steele at UC Irvine. At Yale, Dr. Juliano began working with Hydra, a small freshwater cnidarian that continually renews all cell types as an adult and has remarkable regenerative abilities. During her post-doctoral work, she discovered a critical role for the PIWI-piRNA pathway in Hydra stem cells. In her own laboratory at UC Davis, Dr. Juliano continues to use Hydra as a model to understand, stem cell function, development, and regeneration, with funding from the National Institutes of Health. Dr. Juliano was a recipient of the Elizabeth D. Hay New Investigator award from the Society for Developmental Biology in 2020 and she was named a UC Davis Chancellor’s fellow in 2024. Dr. Juliano is the founder of the biennial Cnidarian Model Systems Meetings, the founder and director of the annual Hydra Workshop (Marine Biological Laboratory), and a founding board member of the International Society for Regenerative Biology. 

Abstract:
In our laboratory at UC Davis, we use Hydra as a model to understand, stem cell function, development, and regeneration. As a starting point, we subjected the adult Hydra to single cell sequencing, created a molecular map of the entire organism, and built differentiation trajectories to describe each stem cell differentiation pathway. This work now serves as a foundation for our research goals, which include dissecting the molecular mechanisms underlying stem cell differentiation, understanding how the conserved injury program triggers developmental pathways during regeneration, and understanding how the Hydra nervous system is able to continually remove and add neurons into neural circuits.

Watch the seminar here!

Dr. Felisa Smith | Smith Lab

Bio:
Felisa Smith is a Distinguished Professor in the department of Biology. A conservation paleoecologist, she integrates modern, historic and fossil mammal records to investigate pressing environmental issues such as climate change and biodiversity loss. Over her career she has worked on organisms from microbes to mammoth, but vastly prefers the latter. Most recently Smith has been using the terminal Pleistocene megafauna extinction as a proxy for understanding modern mammal biodiversity loss. In addition to her 3 books, she has written~120 papers/book chapters in a wide variety of scientific journals, and taught scientific blogging at UNM (http://unm-bioblog.blogspot.com). She has participated in many audio and video programs including National Public Radio, BBC World Service, BBC Earth, and BBC’s Horizon series, German public radio, the Canadian Broadcasting Corporation, and the History Channel as well as numerous print interviews/essays. Felisa was elected a Fellow of the Paleontological Society in 2020, was awarded the Merriam Award from the American Society of Mammalogists in 2022, and is the 68th recipient of the UM Annual Research Lecturership in 2023. She is currently the President of the American Society of Mammalogists and Past President of the International Biogeography Society.

Abstract:
The conservation status of large-bodied mammals is dire. Their decline has serious consequences because they have unique ecological roles not replicated by smaller-bodied animals. Here, we use the fossil record of the megafauna extinction at the terminal Pleistocene to explore the consequences of past biodiversity loss. We characterize the isotopic and body-size niche of a mammal community in Texas before and after the event to assess the influence on the ecology and ecological interactions of surviving species (>1kg). Pre-extinction, a variety of C₄-grazers, C₃-browsers, and mixed-feeders existed, similar to modern African savannas, with likely specialization among the two sabertooth cats for juvenile grazers. Post-extinction, body size and isotopic niche space were lost, and the δ¹³C and δ¹⁵N values of some survivors shifted. We see mesocarnivore release within the Felidae: the jaguar, now an apex carnivore, moved into the specialized isotopic niche previously occupied by extinct cats. Puma, previously absent, became common and lynx shifted towards consuming more C₄-based resources. Lagomorphs were the only herbivores to shift towards C₄ resources. Body size changes from the Pleistocene to Holocene were species-specific, with some animals (deer, hare) becoming significantly larger, and others smaller (bison, rabbits) or exhibiting no change to climate shifts or biodiversity loss. Overall, the Holocene body size-isotopic niche was drastically reduced and considerable ecological complexity lost. We conclude biodiversity loss led to reorganization of survivors and many ‘missing pieces’ within our community; without intervention, the loss of Earth’s remaining ecosystems that support megafauna will likely suffer the same fate.

Dr. Smith at Texas Memorial Museum

Fossils under study

Cave art showing human hunting

Dr. Antonio Lazcano Araujo 

Bio:
Antonio Lazcano is Distinguished Professor at the Universidad Nacional Autónoma de México, where he works on the origin and early evolution of life. He has worked in prebiotic chemistry, analyses of meteorites and, more lately, on bioinformatics and the reconstruction of early stages of celular evolution. He is author or coauthor of about 200 research papers and chapters in books. He has written several boioks for the general public, including El Origen de la Vida, La Chispa de la Vida y La Bacteria Prodigiosa. He has been Visiting Professor or Scholar in Residence at the Univeristy of Habana, Autónoma de Madrid, Houston, Valencia, Orsay Paris-Sud, University of California, San Diego, Universita di Roma La Sapienza, Institut Pasteur, ETH Zentrum in Zurich and the A. N. Bakh Institute of Biochemistry of the USSR. For ten years he was part of the NASA Astrobiology Institute Oversee Committee, and President of the Gordon Research Conference of the Origins of Life, and twice President of the International Society for the Study of the Origins of Life, being so far the only Latin American scientist to hold this position. He has received three Honoris causa, one from the Universita di Milano (Italy, 2008), one from the Universidad de Valencia (Spain, 2014), and a third one in 2015 from the  Universidad de Michoacan (Mexico). In 2013 the Third World Summit of Evolution granted him the Charles Darwin Distinguished Scientist Award, and in 2018 the College de France granted him the Guillaume Bude Medal. In October 2014 he was elected to the Colegio Nacional, the most Mexican important academic and cultural institution.

Abstract:
Led by Oparin’s hypothesis on a heterotrophic origin of life, in the early 1950s Stanley L. Miller began his PhD thesis under the supervision of Harold C. Urey, attempting to simulate the conditions of the primitive Earth. To do this, Miller placed a mixture of methane, ammonia, and hydrogen in a flask, to which water vapor from another flask simulating the primitive seas of the planet was added. After subjecting the mixture of gases to the action of electrical discharges, Miller found that in a very short time amino acids, urea, and other compounds of biochemical importance had been formed. The experiment was considered a demonstration of the premises of Oparin's theory, and marks the origin of the experimental study of the appearance of life. Analyses of the original samples from Miller's experiment using contemporary techniques has shown that the variety of compounds formed abiotically is much greater than originally reported, allowing a more complete picture of the processes that led to the origin of the first organisms.

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Dr. Alex Bisson | Bisson Lab

Abstract:
Cells sense and respond to their physical surroundings, using organized molecular machinery
to convert mechanical environmental signals into biochemical information. Maybe more importantly, little is known about how cells' material properties co-evolve with their
environment. Using genetics, biophysics, and advanced microscopy tools, the Bisson Lab aims to understand archaeal cells' self-organization and behavior in response to physical cues. Here,
I will discuss our recent discovery of how specific mechanical confinement triggers the development from a unicellular to a tissue-like lifestyle similar to known primitive multicellular eukaryotes. This observation not only gives a new perspective over the emergence of complex multicellularity, but gives us the opportunity to compare the behavior and the genome of hundreds of cultivable archaeal species.

Dr. Erica Glasper

Bio:
Erica R. Glasper graduated with honors from Randolph-Macon College in Ashland, Virginia, in 2002 with a major in Psychology and a minor in Biology. Initially pre-med, Erica discovered neuroscience during her freshman year at Randolph-Macon and was selected three times as a Summer Undergraduate Research Fellow. Her research experiences, aided by keen faculty mentorship, set her professional journey in motion. Erica went on to earn an M.A. and Ph.D. in Psychobiology and Behavioral Neuroscience from The Ohio State University. During her time as a postdoctoral scholar at Princeton University, she was supported by a fellowship from the UNCF/Merck Science Initiative and the National Institute on Aging at the National Institutes of Health. In 2011, Dr. Glasper joined the faculty at the University of Maryland – College Park, in the Department of Psychology, as an Assistant Professor. Her research in behavioral neuroendocrinology takes a multidisciplinary approach to understanding how experiences can shape our brains and resulting behavior. Following success as a researcher and educator, she was awarded tenure and promoted to the rank of Associate Professor. During the summer of 2021, the Glasper Lab returned to The Ohio State University, where she joined the Department of Neuroscience and the Institute for Behavioral Medicine Research within the College of Medicine as a tenured Associate Professor. She is excited about continued research success, and her return to the Buckeye State, using a combination of behavioral paradigms along with neuroendocrine, neuroanatomical, neuroimmune, neurochemical, and pharmacological techniques in three lines of research: 1) neurobiology of parenting, 2) neuroprotective role of rewarding social experiences, and 3) enduring consequences of paternal deprivation. Her research is currently funded by the NIH and The Ohio State University Wexner Medical Center.

Abstract:
Loss of a mate results in diverse impairments in bodily and psychological health. In this study, we tested the hypothesis that disrupting a mate bond, in the monogamous California mouse (Peromyscus californicus), would increase the neuroimmune response to a peripheral inflammatory stimulus (lipopolysaccharide [LPS]) through alterations in the oxytocin system. Adult (6-8 months old) male and female mice were exposed to three experimental conditions: 1) single housed, 2) mate bonded, or 3) mate-bonded separation. Mice were either injected with a vehicle (VEH) or an intraperitoneal injection of LPS (1mg/kg) and sacrificed 4-6 hours later.  While mate bond disruption did not increase anxiety-like behavior during open-field testing, physiological indices of mate bond disruption were observed. Males lost significantly more body weight following mate-bond separation, compared to the mate-bonded groups – this effect was not observed in females. Pro-inflammatory cytokine concentration (TNF and IL-1 beta) mRNA levels, measured by RT-qPCR in the hippocampus (HIPP) and hypothalamus (HYPO), were significantly enhanced in LPS-treated female mice following mate bond disruption, compared to the mate-bonded group. Mate bond dissolution did not exacerbate the LPS-induced increase in pro-inflammatory cytokines in males. Disruptions in oxytocin (OXT) signaling may contribute to the increased pro-inflammatory response in LPS-injected mice following mate bond dissolution, as HIPP mRNA levels for the oxytocin receptor (OXTR) in separated males and females were significantly decreased. Independent of endotoxic challenge, TNF and OXTR mRNA levels in separated mice were negatively correlated (as OXTR expression went down, TNF expression went up). Together, these results suggest that the effects of mate bond disruption in neuroimmune responsivity may involve alterations to OXT signaling. 

Watch the seminar here!