Jonathan Gitlin

Emeritus Senior Scientist

Jonathan Gitlin headshot
Contact Information
Education
M.D., Medicine (cum laude), University of Pittsburgh School of Medicine, 1978
B.S., Biochemistry (cum laude), University of Pittsburgh, 1974
MBL Affiliation
Bell Center
Research Area
Developmental Biology
Models of Human Disease
Regeneration

Jonathan Gitlin is an American pediatrician specializing in early human development and genetics and recognized for his research in human nutrition.  Prior to joining the ǧƵ, he was on the faculty at Harvard Medical School, Washington University School of Medicine and Vanderbilt University where he was the James C. Overall Professor & Chair of the Department of Pediatrics. He is currently a Senior Scientist Emeritus at Marine Biological Laboratory, where he served as both the Director of the Eugene Bell Center and as Director of Research.  Dr. Gitlin is the author of more than 150 papers and has received numerous professional honors. He is an elected fellow of the AAAS and a member of the National Academy of Medicine.

Research efforts in the laboratory have focused on the interplay of the environment and the genome in early human development as a model for understanding  human disease, environmental adaptation and evolutionary biodiversity. 

Elucidation of the genetic basis of the disorders of human copper metabolism revealed the evolutionarily conserved mechanisms of copper trafficking and compartmentalization within cells and defined the unique role of copper in synaptic plasticity and neuronal injury. Similarly, genetic studies of iron metabolism in our lab revealed the essential physiologic role of ceruloplasmin in iron homeostasis and neuronal survival in the developing central nervous system. More recently, studies utilizing zebrafish as a model for early development revealed an evolutionarily conserved developmental hierarchy of copper metabolism that is informed by specific genetic factors, providing a novel paradigm for the role of suboptimal nutrition in the pathogenesis of human birth defects. 

Current studies are focused on energy homeostasis during early development and the genetic basis for the biochemical adaptations to oxygen availability in extreme environments that are a fundamental aspect of evolutionary biology. (see Life Interrupted: Exploring the World of Extreme Adaptation)

Selected Publications

Soma S, Latimer AJ, Chun H, Vicary AC, Timbalia SA, Boulet A, Rahn JJ, Chan SSL, Leary SC, Kim BE, Gitlin JD, Gohil VM. Elesclomol restores mitochondrial function in genetics models of copper deficiency. Proc Natl Acad Sci 2018; 11: 8161-8166. PMCID: 

Kumar D, Thomason RT, Yankova M, Gitlin JD, Mains RE, Eipper BA, King SM. Microvillar and ciliary defects in zebrafish lacking an actin-binding bioactive peptide amidating enzyme. Sci Rep 2018: 8:4547.  PMCID: 

Copper homeostasis: specialized functions of the late secretory pathway. Dev Cell 2014; 29:631-632.  DOI: 

Wang Y, Zhu S, Weisman GA, Gitlin JD, Petris MJ. Conditional knockout of the Menkes disease copper transporter demonstrates its critical role in embryogenesis. PloS One 2012; 7:e43039. PMCID: 

van Boxtel AL, Gansner JM, Hakvoort HWJ, Snell H, Legler J, Gitlin JD. Lysyl oxidase like 3b is critical for cartilage maturation during zebrafish craniofacial development. ѲٰDZDz2011; 30:178-187. PMCID: 

Mendelsohn BA, Kassebaum BL, Gitlin JD. The zebrafish embryo as a dynamic model of anoxia tolerance. Dev Dyn 2008; 237:1780-1788.  PMCID: 

Thiele DJ, Gitlin JD. Transition Metal Metabolism: Assembling the Pieces. Nature Chem Biol 2008; 4:145-147. PMCID: 

Madsen EC, Morcos PA, Mendelsohn BA, Gitlin JD. In vivo correction of a Menkes disease Madsen EC, Morcos PA, Mendelsohn BA, Gitlin JD.  Proc Natl Acad Sci 2008; 105; 3909-3914. PMCID: 

Madsen E, Gitlin JD. Copper and Iron Disorders of the Brain. Annual Review Neuroscience 2007; 30:317-337.   DOI:

Mendelsohn BA, Yin C, Johnson SL, Wilm T, Solnica-Krezel L, Gitlin JD. Atp7a determines a hierarchy of copper metabolism essential for notochord development. Cell Metabolism  2006; 4:155-162.  DOI: