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Faculty Detail     Name BRADLEY K YODER   Campus Address MCLM 688 Zip 0006 Phone 205-934-0994 E-mail byoder@uab.edu Other websites

Faculty Appointment(s) Appointment Type Department Division Rank Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor Center  Arthritis & Musculoskeletal Diseases Center  Arthritis & Musculoskeletal Diseases Center Professor Center  Pathology   Cell Adhesion & Matrix Research Center Professor Center  Center for Aging  Center for Aging Professor Center  Center for Metabolic Bone Disease  Center for Metabolic Bone Disease Professor Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor Center  Medicine  Comprehensive Diabetes Ctr Professor Center  Cystic Fibrosis Research Center  Cystic Fibrosis Research Center Professor Center  Medicine  Nephrology Res & Trng Ctr Professor

Graduate Biomedical Sciences Affiliations Cell, Molecular, & Developmental Biology  Cellular and Molecular Biology Program  Genetics and Genomic Sciences  Hughes Med-Grad Fellowship Program  Integrative Genetics Graduate Program  Medical Scientist Training Program  Pathobiology and Molecular Medicine

Biographical Sketch  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.

Society Memberships Organization Name Position Held Org Link American Society of Cell Biology    http://www.ascb.org/  American Society of Nephrology    http://www.asn-online.org/  National Kidney Foundation    http://www.kidney.org/  Society for Developmental Biology    http://www.sdbonline.org/

Research/Clinical Interest Title Cilia Signaling and Dysfunction in Development and Disease 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 phenotypes. 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?

Selected Publications  Publication PUBMEDID Kierszenbaum AL, Rivkin E, Tres LL, Yoder BK, Haycraft CJ, Bornens M, Rios RM. GMAP210 and IFT88 are present in the spermatid golgi apparatus and participate in the development of the acrosome-acroplaxome complex, head-tail coupling apparatus and tail. Dev Dyn. 240(3):723-36, (2011).  21337470  O'Connor AK, Kesterson RA, Yoder BK. Generating conditional mutants to analyze ciliary functions: the use of cre-lox technology to disrupt cilia in specific organs. Methods Cell Biol. 2009;93:305-30. Epub 2009 Dec 4.  20409823  Lehman JM, Laag E, Michaud EJ, Yoder BK. An essential role for dermal primary cilia in hair follicle morphogenesis.J Invest Dermatol. 2009 Feb;129(2):438-48. Epub 2008 Nov 6.   20362090  Kesterson RA, Berbari NF, Pasek RC, Yoder BK. Utilization of conditional alleles to study the role of the primary cilium in obesity. Methods Cell Biol. 2009;94:163-79. Epub 2009 Dec 23.   20362090   Williams CL, Masyukova SV, Yoder BK. Normal ciliogenesis requires synergy between the cystic kidney disease genes MKS-3 and NPHP-4.J Am Soc Nephrol. 2010 May;21(5):782-93. Epub 2010 Feb 11.  20150540  Schneider L, Cammer M, Lehman J, Nielsen SK, Guerra CF, Veland IR, Stock C, Hoffmann EK, Yoder BK, Schwab A, Satir P, Christensen ST.Directional cell migration and chemotaxis in wound healing response to PDGF-AA are coordinated by the primary cilium in fibroblasts. Cell Physiol Biochem. 2010;25(2-3):279-92.  20110689  Clement CA, Kristensen SG, Møllgård K, Pazour GJ, Yoder BK, Larsen LA, Christensen ST. The primary cilium coordinates early cardiogenesis and hedgehog signaling in cardiomyocyte differentiation. J Cell Sci. 2009 Sep 1;122(Pt 17):3070-82. Epub 2009 Aug 4.  19654211   Clement CA, Kristensen SG, Møllgård K, Pazour GJ, Yoder BK, Larsen LA, Christensen ST. The primary cilium coordinates early cardiogenesis and hedgehog signaling in cardiomyocyte differentiation. J Cell Sci. 2009 Sep 1;122(Pt 17):3070-82. Epub 2009 Aug 4.  19654211   Berbari NF, O'Connor AK, Haycraft CJ, Yoder BK.The primary cilium as a complex signaling center, Curr Biol. 2009 Jul 14;19(13):R526-35.   19602418   Veland IR, Awan A, Pedersen LB, Yoder BK, Christensen ST. Primary Cilia and Signaling Pathways in Mammalian Development, Health and Disease. Nephron Physiol. 2009 Mar 10;111(3):p39-p53  19276629   First Prev   1 2 3 4 5 6 7 of  7  Next Last

Keywords Cilia, cystic kidney diseases, obesity, signal transduction, cell fate determination and embryonic patterning, birth defects, mouse and C. elegans models.

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