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Faculty Detail Faculty Entry   
Name BRADLEY K YODER  
Campus Address MCLM 688 Zip 0006
Phone 205-934-0994
E-mail byoder@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:byoder@uab.edu">byoder@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
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  Med - Nephrology Professor
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor

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?

Postdoc Positions Available
Date Posted Position Title
05/01/2011  Postdoctoral Research Fellow 
A Postdoctoral position is available to study the importance of cilia in development, disease, and normal cellular physiology. The lab utilizes comparative approaches in both mouse and C. elegans to explore how the cilium is constructed and maintained and to determine its role in signal reception and transmission in relation to disease states and developmental abnormalities. Emphasis is on ciliary functions on renal and neuronal cells in adult mice, and in hair follicle and skin development. If interested or if you have additional questions please contact Dr. Bradley Yoder at byoder@uab.edu. Postdoctoral fellows with experience with C. elegans or with expertise in biochemistry or genetics are encouraged to apply.
   
 

Selected Publications 
Publication PUBMEDID
P. Darwin Bell, Wayne Fitzgibbon, Antine Stenbit, Sandra Gilley, Amber Houston, Kelli Sas, May Amria, Gene P. Siegal, John Bissler, Mehmet Bilgen, Peter Cheng-te Chou, Lisa Guay-Woodford, Bradley K. Yoder, Courtney J. Haycraft Ryan Reichert, and Brian Siroky. Interactions between Cilia, Hypertrophic Signaling, and Renal Cystogensis. Journal of American Society for Neprhology, (2011). PMCID: PMC3083306  3083306 
Edward J Michaud and Bradley K Yoder. Soluble levels of cytosolic tubulin coordinate ciliary length control. Molecular Biol. of the Cell. 22(6):806-16, (2011).   3057705 
Corey L. Williams, Chunmei Li, Katarzyna Kida, Peter N. Inglis, Swetha Mohan, Lucie Semenec, Nathan J. Bialas, Rachel Stupay, Nansheng Chen, Oliver E. Blacque*, Bradley K. Yoder*, and Michel R. Leroux*. MKS and NPHP functional modules establish basal body/transition zone-membrane associations and ciliary gate function during ciliogenesis. *Co-corresponding authors. Journal of Cell Biol. 192(6):1023-41. (2011)  3063147 
Mandy J. Croyle, Jonathan M. Lehman, Amber K. O’Connor, Sunny Y Wong, Erik B. Malarkey, Daniela Iribarne, William E. Dowdle, Trenton R. Schoeb, Zoe M. Verney, Mohammad Athar Edward J. Michaud, Jeremy F. Reiter, and Bradley K. Yoder. Role of Epidermal Primary Cilia in the Homeostasis of Skin and Hair Follicles. Development. 138(9):1675-85 (2011).  3074444 
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 
Anastasia D. Egorova, Padmini P.S.J. Khedoe, Marie-Jose T.H. Goumans, Bradley K Yoder, Surya M. Nauli, Peter ten Dijke, Robert E. Poelmann, and Beerend P. Hierck. Lack of primary cilia primes shear-induced Endothelial-to-Mesenchymal Transition. Circulation Research, 108(9):1093-101 (2011).  3094764 
Svetlana V. Masyukova, Marlene E. Winkelbauer, Corey L. Williams, Jay N. Pieczynski, and Bradley K. Yoder Assessing the pathogenic potential of human Nephronophthisis disease-associated NPHP-4 missense mutations in C. elegans. Human Molecular Genetics 20:2942-2954. (2011)   3131040 
Nicolas F. Berbari, Nicholas W. Kin, Neeraj Sharma, Edward J. Michaud, Robert A. Kesterson, and Bradley K. Yoder. Mutations in Traf3ip1 reveal defects in ciliogenesis, embryonic development, and altered cell size regulation. Developmental Biology (in press 2011).    
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.
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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.
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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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