Nature has created many powerful biomolecules that are hidden in organisms across kingdoms of life. Many of these biomolecules originate from microbes, which contain the most diverse gene pool among living organisms. We are integrating high-throughput computational and experimental approaches to harness the vast diversity of genes in microbes to develop new antibiotics and molecular biotechnology, and to investigate the evolution of proteins and molecular mechanisms in innate immunity.
Dr. Rutaganira uses choanoflagellates—the closest living single-celled relatives to animals—to study the origin of animal cell communication. Dr. Rutaganira applies chemical, genetic, and cell biological tools to probe choanoflagellate cell-cell communication, with implications for understanding not only animal cell signaling, but also the origin of multicellularity in animals.
PhD in Biochemistry (University of California San Francisco)
We study the biology of chromosomes broadly defined. Our work focuses on understanding the genetic and epigenetic control of chromosome organization and function. We use a combination of cell biology, biochemistry, microscopy, computation, and functional genomics in our laboratory to address questions in chromosome biology. Specifically, we are interested in the assembly and function of the centromere and kinetochore, RNA dependent regulation of chromatin epigenetic states, the function of repetitive elements in genomes and the physical organization of chromosomes.
Current Lab Members
PhD in Biochemistry (Stanford University)
Over the last several decades the Spudich laboratory studied the structure and function of the myosin family of molecular motors in vitro and in vivo, and we developed multiple new tools, including in vitro motility assays taken to the single molecule level using laser traps. That work led us to our current focus on the human cardiac sarcomere and the molecular basis of hypertrophic and dilated cardiomyopathy. We postulated in 2015 that a majority of hypertrophic cardiomyopathy mutations are likely to be shifting b-cardiac myosin heads from a sequestered off-state to an active on-state for interaction with actin, resulting in the hypercontractility seen clinically in hypertrophic cardiomyopathy patients. This hypothesis is different from earlier prevailing views, and this viewing an old disease in a new light is the basis of our current research.