The night will consist of networking and a presentation by student-invited keynote speaker Dr. Benjamin R. Myers (Associate Professor of Oncological Sciences at the University of Utah School of Medicine).

Two full days of scientific talks, poster presentations, and roundtable discussions will be hosted on October 29th and 30th at Nicholson Tower Conference Center . We are honored to host talks throughout the two days by invited speakers: Susan Dutcher (Professor of Genetics and Cell Biology and Physiology at Washington University School of Medicine), Brad Yoder (Professor of Cell, Developmental, and Integrative Biology at the University of Alabama at Birmingham), Eva Anton (Professor of Cell Biology and Physiology and member of the Neuroscience Center at the University of North Carolina at Chapel Hill), Julie Siegenthaler (Associate Professor of Pediatric Developmental Biology at the University of Colorado, Anschutz), Denise Ferkey (Associate Professor of Biological Sciences at the University at Buffalo), Anand Swaroop (Senior Investigator of Neurobiology, Neurodegeneration & Repair at the National Eye Institute). Local experts and selected Cell Biology graduate students will present talks alongside invited speakers.

Ben Myers, PhD

Dr. Ben Myers is an Associate Professor of Oncological Sciences and Adjunct Associate Professor of Biomedical Engineering and Biochemistry at the University of Utah. His work focuses on cellular communication with particular focus on the Hedgehog pathway, GPCR signaling, and the role of lipids in these processes. His lab utilized computational approaches alongside biochemical and functional experimentation to tease apart these mechanisms and their role in pathology. In a recently published Nature Structural and Molecular Biology study, he investigated the role of intrinsically disordered regions in the Smoothened/PKA-C interaction, uncovering a structural mechanism for this key step in Hedgehog signaling.

Susan Dutcher, PhD

Dr. Susan Dutcher is a Professor of Genetics at Washington University in St. Louis. She was inducted to the National Academy of Sciences in 2025. Her work focuses on how cilia assemble and the influence of genetics on ciliary function using comparative genetics, bioinformatics, microscopy, and biochemistry. She utilizes the unicellular algae Chlamydomonas alongside human cell culture to pursue questions of basic ciliary biology and delve into dysfunction underlying Primary Ciliary Dyskinesia. In a recent publication, she showed that loss of the PCD-linked proteins CCDC39 and CCDC40 results in loss of a large structural protein network in cilia with significant functional consequences.

Brad Yoder, PhD

Dr. Brad Yoder is the Chair of Developmental and Integrative Biology at the University of Alabama at Birmingham. His lab focuses on primary cilia formation, maintenance, and function. His work covers topics such as intraflagellar transport, cellular sensation, motility, and signaling. The Yoder lab utilizes C. elegans and mice to study cilia formation and function in animal behavior, mammalian development, and cystic kidney disease.

Eva Anton, PhD

Dr. Eva Anton is a Professor in the Department of Cell Biology and Physiology at UNC-Chapel Hill. He is a well accomplished scientist in the field of neurobiology and cilia biology. His lab investigates the molecular mechanisms of neural progenitor differentiation, migration, and connectivity using a variety of tools, including mouse genetics and advanced imaging techniques. Particularly, he is interested in the role of primary cilia in the regulation of the processes mentioned above. In a recent study, he comprehensively characterized the primary cilia that protrude from neurons and astrocytes in the cerebral cortex, revealing the characteristics of cilia in astrocytes/neurons as well as their participation in the synapses.

Julie Siegenthaler, PhD

Dr. Julie Siegenthaler is an Associate Professor of Pediatric Developmental Biology at the University of Colorado, Anschutz. She is a neuroscientist whose work focuses on understanding the interplay between the central nervous system (CNS) and its support structures (the meninges and brain vasculature). Her lab integrates a variety of technical approaches including advanced imaging, multi-omics, and molecular assays to better understand how the meninges and vasculature actively shape how the brain develops and functions. Her recent research has investigated how meningeal-derived retinoic acid signaling controls neural development by influencing Notch and Sox2. Her lab also studies how these support structures influence response to injury, inflammation, and disease of the CNS.

Denise Ferkey, PhD

Dr. Denise Ferkey is an Associate Professor in the Department of Biological Sciences at the University at Buffalo. She is a neuroscientist and sensory biologist who studies how the nervous system detects environmental cues and modulates signaling to control behavior. Her lab uses C. elegans and its chemosensory pathways to investigate how nerve cells process sensory signals. For example, her research has examined how arginine methylation of G protein-coupled receptors (GPCRs) regulates G protein signaling. This work has identified potential targets that could contribute to a better understanding and treatment of nervous system disorders.

Anand Swaroop, PhD

Dr. Anand Swaroop is a Senior Investigator in Neurobiology, Neurodegeneration & Repair and in Retinal Development, Genetics & Therapy at the National Eye Institute. His work focuses on understanding how photoreceptors develop, age, and become damaged during retinal disease, as well as developing new treatments for photoreceptor dysfunction. His recent research has sought to identify gene regulatory networks that influence photoreceptor differentiation, define cellular pathways and genetic variants that contribute to photoreceptor degeneration, and develop gene- and cell-based therapies targeting these pathways. His work ultimately aims to translate a deeper understanding of photoreceptor biology into new therapeutic strategies for retinal degenerative diseases.