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Bradley Yoder, PhD

Bradley Yoder, PhD
 
Professor
Dept. of Cell Biology
Office Address: MCLM 652
Phone: 205-934-0994
E-mail: byoder@uab.edu
Web Site


Dr. Bradley K. Yoder (b. 1966), Professor , completed his undergraduate studies in biochemistry and molecular biology at the University of Maryland Baltimore County (B.S. 1988), and received a Ph.D. in molecular and cellular biology from the University of Maryland in 1993. His postdoctoral studies were performed at Oak Ridge National Laboratory under the guidance of Dr. Rick Woychik where Dr. Yoder was an Alexander Hollaender Distinguished Postdoctoral Fellow. His research over the past two decades has focused on the cellular and molecular mechanisms regulating assembly, maintenance, and function of the primary cilium utilizing complementary approaches in mice, C. elegans, and in cell culture models. Work from his laboratory has utilized genetic screens in C. elegans to identify proteins required for ciliogenesis and cilia mediated signaling activities and how these genes function in pathways (e.g. Daf-2 Insulin/IGF-like pathway) that regulate life span and energy homeostasis. His group has analyzed in mammalian systems how the cilium regulates important developmental pathways and how loss of the cilium causes abnormalities in left-right body axis specification, limb and tooth patterning, skin and hair follicle morphogenesis, and impairs endochondrial bone formation. His group is also providing important fundamental insights into the connection between ciliary dysfunction and cystic kidney disorders, and novel roles for neuronal cilia in the regulation of satiation responses, disruption of which causes obesity and type II diabetes.

Education:

University of Maryland Baltimore County
BA, Biochemistry and Molecular Biology, 1988

University of Maryland
PhD, Molecular and Cellular Biology, 1993

Research Description:

Cilia are microtubule based structures that can be motile or immotile, the latter being referred to as primary cilia. In contrast to motile cilia, such as those found on epithelia of the trachea, the importance of the primary cilium is relatively undefined despite their presence on most mammalian cells. Cilia are extremely complex organelles which are devoid of ribosomes, thus, proteins required for cilia assembly, maintenance, and signaling must be imported into the cilium. This occurs through a microtubule-based transport system called intraflagellar transport (IFT). Proteins involved in IFT concentrate around the basal body at the base of the cilium and assemble into complexes (IFT particles) which are moved up the cilium by a kinesin and returned by a cytoplasmic dynein. The IFT particle is thought to mediate the transport of cargo into the cilium as well as to deliver signals initiated in the cilium to the cytosol. Although the primary cilium was once thought to be a vestigial organelle, recent studies have uncovered that cilia in mammals are required for viability and that dysfunction of the cilium is associated with a large number of developmental abnormalities and disease pathologies. This now includes obesity, cystic kidney, liver, and pancreatic diseases, hydrocephalus, skin and hair follicle abnormalities, random left-right body access specification, and skeletal defects. Although studies in mice and humans now indicate that cilia are critically important organelles, the functions of cilia and the pathways in which they are required remains largely unknown. Addressing these issues is the major focus of my group's research. Our studies utilize comparative approaches in both mouse and C. elegans to investigate four major interrelated themes:

  1. What roles do cilia play in regulating signaling pathways?
  2. What are the functions of cilia in embryogenesis and tissues physiology in postnatal life?
  3. How does cilia dysfunction cause disease and developmental abnormalities?
  4. What proteins localize in cilia, how are they targeted to this organelle, and what role do they play in cilia assembly or signaling activities?