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Faculty Detail    
Name BRADLEY K YODER
Director Cell, Molecular, and Developmental Biology Graduate Theme
Director T32 Training Program in Cell and Molecular Biology
Director, P30 Hepatorenal Fibrocystic Disease Core Center
 
Campus Address THT 926A Zip 0006
Phone  (205) 934-0994
E-mail  byoder@uab.edu
Other websites
     


Faculty Appointment(s)
Appointment Type Department Division Rank
Center  Comp Arthritis, MSK, Bone & Autoimmunity Ctr  Comp Arthritis, MSK, Bone & Autoimmunity Ctr Professor
Center  Comprehensive Diabetes Center  Comprehensive Diabetes Center Professor
Center  Comprehensive Cancer Center  Comprehensive Cancer Center Professor
Center  Integrative Center for Aging Research  Integrative Center for Aging Research Professor
Center  Cystic Fibrosis Research Center  Cystic Fibrosis Research Center Professor
Center  General Clinical Research Center  Nephrology Research & Training Center Professor
Center  GL Ctr for Craniofacial, Oral, & Dental Disorders  GL Ctr for Craniofacial, Oral, & Dental Disorders Professor
Center  Vision Sciences (Org-Ret)  Vision Science Research Center (Org-Ret) Professor
Center  Nutrition Sciences   Nutrition Obesity Res Ctr (NORC) Professor
Center  Pathology   Cell Adhesion & Matrix Research Center Professor
Primary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Professor

Graduate Biomedical Sciences Affiliations
Cell, Molecular, & Developmental Biology 
Cellular and Molecular Biology Program 
Genetics, Genomics and Bioinformatics 
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 come in both motile and immotile forms. While motile cilia were known to have important roles in the lung and respiratory system, primary cilia were largely considered vestigial structures. A major paradigm shift in the field occurred with the generation of mouse mutants (such as the orpk mouse) that disrupt cilia formation. These new mouse mutants revealed important and novel roles for motile and immotile cilia and demonstrated that they are essential for development and tissue function. Defects in cilia have been implicated as the cause of a large and rapidly expanding group of human syndromes (Ciliopathies) with a wide range of developmental and disease phenotypes. The objectives of my research program are to uncover mechanisms regulating assembly, maintenance, and functions of both motile and primary forms of cilia and to determine how defects in these processes contribute to developmental abnormalities and disease pathogenesis. To accomplish these goals, my group utilizes complementary cell, genetic, and biochemical approaches in mice, C. elegans, and cell culture to identify new proteins involved in ciliogenesis and cilia mediated signaling. Work from my group has identified novel components of the ciliary transition zone, an important domain controlling what protein enter or are retained in the cilium. We have provided seminal insights into how the cilium regulates developmental pathways, such as hedgehog, and how alterations in cilia-mediated regulation of this pathway cause polydactyly, defects in endochondral bone formation, and abnormal skin and hair follicle morphogenesis. My group made fundamental contributions that connected ciliary dysfunction to the formation of cysts in the kidney, liver, and pancreas, and uncovered a new role for cilia on hypothalamic neurons in regulating satiation responses. We have shown that disruption of cilia on these neurons cause morbid obesity and type II diabetes. We also identified genes important in regulating ciliary motility and waveform and determined that their loss in mice leads to hydrocephalus, bronchiectasis, and randomization of the left-right body axis. Importantly, as part of this work we determined that a mutation of one of these genes we identified in our mouse model is responsible for a form of primary ciliary dyskinesia (PCD) in humans. As in the mouse model, these human PCD patients frequently have left-right body situs defects. In summary, the research conducted by my group is providing important and innovative insights into how cilia are constructed and how they are established as a unique signaling and sensory organelle with a distinct protein composition the rest of the cell membrane. We have uncovered many diverse and unexpected roles for cilia during development and in maintaining mammalian health.

Selected Publications 
Publication PUBMEDID
MB Hovater, D Olteanu, EL Hanson, NL Cheng, B Siroky, A Fintha, P Komlosi, W Liu, LM Satlin, PD Bell, BK Yoder, EM Schwiebert. Loss of apical monocilia on collecting duct principal cells impairs ATP secretion across the apical cell surface and ATP-dependent and flow-induced calcium signals. Purinergic Signal. 2008 Jun;4(2):155-70.  18368523  
ET Johnson, T Nicola, K Roarty, BK Yoder, CJ Haycraft, R Serra. Role for primary cilia in the regulation of mouse ovarian function. Dev Dyn. Aug;237(8):2053-60. (2008)   18629867  
SK Nielsen, K Møllgård, CA Clement, IR Veland, A Awan, BK Yoder, I Novak, ST Christensen. Characterization of primary cilia and Hedgehog signaling during development of the human pancreas and in human pancreatic duct cancer cell lines. Dev Dyn. 237(8):2039-52. 2008  18629868  
J Lehman, E Laag, MJ Michaud, BK Yoder. An Essential Role for Dermal Primary Cilia in Hair Follicle Morphogenesis. Journal of Investigative Dermatology, Feb;129(2):438-48. (2009)  18987668  
Sharma N, Berbari NF, Yoder BK. Ciliary dysfunction in developmental abnormalities and diseases. Curr Top Dev Biol.;85:371-427. (2008)  19147012  
Sharma N, Berbari NF, Yoder BK. Ciliary dysfunction in developmental abnormalities and diseases. Curr Top Dev Biol. 2008;85:371-427  19147012  
Ohazama A, Haycraft CJ, Seppala M, Blackburn J, Ghafoor S, Cobourne M, Martinelli DC, Fan CM, Peterkova R, Lesot H, Yoder BK, Sharpe PT. Primary cilia regulate Shh activity in the control of molar tooth number. Development. Mar;136(6):897-903. (2009)  19211681  
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  
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  
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  
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 
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 
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  
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 
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 
Increased Na+/H+ exchanger activity on the apical surface of a cilium-deficient cortical collecting duct principal cell model of polycystic kidney disease.
Olteanu D, Liu X, Liu W, Roper VC, Sharma N, Yoder BK, Satlin LM, Schwiebert EM, Bevensee MO.
Am J Physiol Cell Physiol. 2012 May 15;302(10):C1436-51. doi: 10.1152/ajpcell.00063.2011. Epub 2012 Feb 1. 
22301060  
Kidney injury accelerates cystogenesis via pathways modulated by heme oxygenase and complement.
Zhou J, Ouyang X, Schoeb TR, Bolisetty S, Cui X, Mrug S, Yoder BK, Johnson MR, Szalai AJ, Mrug M.
J Am Soc Nephrol. 2012 Jul;23(7):1161-71. doi: 10.1681/ASN.2011050442. Epub 2012 Apr 19. 
22518005  
Gene therapy rescues cilia defects and restores olfactory function in a mammalian ciliopathy model.
McIntyre JC, Davis EE, Joiner A, Williams CL, Tsai IC, Jenkins PM, McEwen DP, Zhang L, Escobado J, Thomas S, Szymanska K, Johnson CA, Beales PL, Green ED, Mullikin JC; NISC Comparative Sequencing Program, Sabo A, Muzny DM, Gibbs RA, Attié-Bitach T, Yoder BK, Reed RR, Katsanis N, Martens JR.
Nat Med. 2012 Sep;18(9):1423-8. 
22941275  
Mammalian Clusterin associated protein 1 is an evolutionarily conserved protein required for ciliogenesis.
Pasek RC, Berbari NF, Lewis WR, Kesterson RA, Yoder BK.
Cilia. 2012 Nov 1;1(1):20. doi: 10.1186/2046-2530-1-20. 
23351563 
Proximal tubule proliferation is insufficient to induce rapid cyst formation after cilia disruption.
Sharma N, Malarkey EB, Berbari NF, O'Connor AK, Vanden Heuvel GB, Mrug M, Yoder BK.
J Am Soc Nephrol. 2013 Feb;24(3):456-64. doi: 10.1681/ASN.2012020154. Epub 2013 Feb 14. 
23411784  
Quantitative peptidomics of Purkinje cell degeneration mice.
Berezniuk I, Sironi JJ, Wardman J, Pasek RC, Berbari NF, Yoder BK, Fricker LD.
PLoS One. 2013 Apr 8;8(4):e60981. doi: 10.1371/journal.pone.0060981. Print 2013.
PMID: 23593366 Free PMC Article 
23593366  
Leptin resistance is a secondary consequence of the obesity in ciliopathy mutant mice.
Berbari NF, Pasek RC, Malarkey EB, Yazdi SM, McNair AD, Lewis WR, Nagy TR, Kesterson RA, Yoder BK.
Proc Natl Acad Sci U S A. 2013 May 7;110(19):7796-801. doi: 10.1073/pnas.1210192110. Epub 2013 Apr 18 
23599282 
An inducible CiliaGFP mouse model for in vivo visualization and analysis of cilia in live tissue.
O'Connor AK, Malarkey EB, Berbari NF, Croyle MJ, Haycraft CJ, Bell PD, Hohenstein P, Kesterson RA, Yoder BK.
Cilia. 2013 Jul 3;2(1):8. doi: 10.1186/2046-2530-2-8. 
23819925  
Deletion of airway cilia results in noninflammatory bronchiectasis and hyperreactive airways.
Gilley SK, Stenbit AE, Pasek RC, Sas KM, Steele SL, Amria M, Bunni MA, Estell KP, Schwiebert LM, Flume P, Gooz M, Haycraft CJ, Yoder BK, Miller C, Pavlik JA, Turner GA, Sisson JH, Bell PD 
24213915  
Monitoring endosomal trafficking of the g protein-coupled receptor somatostatin receptor 3.
Tower-Gilchrist C, Styers ML, Yoder BK, Berbari NF, Sztul E.
Methods Enzymol. 2014;534:261-80. doi: 10.1016/B978-0-12-397926-1.00015-9 
24359959 
Robert J. Isfort, Dave B. Cody, William G. Richards, Bradley K. Yoder, J. Erby Wilkinson, and Richard P. Woychik. Characterization of growth factor responsiveness and alterations in growth factor homeostasis involved in the tumorigenic conversion of mouse oval cells. Growth Factors 15(2): 81-94, (1998).   
Primary cilia enhance kisspeptin receptor signaling on gonadotropin-releasing hormone neurons.
Koemeter-Cox AI, Sherwood TW, Green JA, Steiner RA, Berbari NF, Yoder BK, Kauffman AS, Monsma PC, Brown A, Askwith CC, Mykytyn K.
Proc Natl Acad Sci U S A. 2014 Jul 15;111(28):10335-40. doi: 10.1073/pnas.1403286111. Epub 2014 Jun 30. 
24982149  
Hippocampal and cortical primary cilia are required for aversive memory in mice.
Berbari NF, Malarkey EB, Yazdi SM, McNair AD, Kippe JM, Croyle MJ, Kraft TW, Yoder BK.
PLoS One. 2014 Sep 3;9(9):e106576. doi: 10.1371/journal.pone.0106576. eCollection 2014. 
25184295  
High-throughput genome editing and phenotyping facilitated by high resolution melting curve analysis.
Thomas HR, Percival SM, Yoder BK, Parant JM.
PLoS One. 2014 Dec 11;9(12):e114632. doi: 10.1371/journal.pone.0114632. eCollection 2014. Erratum in: PLoS One. 2015;10(2):e0117764. 
25503746 

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