Steven M. Claypool, PhD
Highlights
Languages
- English
Gender
MaleJohns Hopkins Affiliations:
- Johns Hopkins School of Medicine Faculty
About Steven M. Claypool
Primary Academic Title
Professor of Physiology
Background
Dr. Steven Michael Claypool is a professor of physiology at the Johns Hopkins University School of Medicine. His research focuses on mitochondrial lipid metabolism and the contribution of phospholipids in mitochondrial function and dysfunction.
Dr. Claypool received his B.A. in biological sciences and his M.A. in molecular, cellular and developmental biology from the University of California, Santa Barbara. He earned a Ph.D. in immunology from Harvard University and performed a postdoctoral fellowship in mitochondrial biology at University of California, Los Angeles.
He has authored or co-authored several peer-reviewed publications, and has presented his work extensively.
Centers and Institutes
X (Twitter)
Recent News Articles and Media Coverage
Fat Molecule’s Inability to Bond with Shape-Shifting Protein in Cell’s Powerhouse Linked to an Inherited Metabolic Disease | Johns Hopkins Medicine, Johns Hopkins Medicine
Additional Academic Titles
Professor of Genetic Medicine
Research Interests
Mitochondrial phospholipid metabolism in health and disease
Lab Website
Steven Claypool Lab - Lab Website
- Research in the Claypool Lab is focused on defining how lipids and membrane proteins interact to establish and maintain normal mitochondrial function and how derangements in this complex relationship result in pathophysiology. We have demonstrated that yeast lacking tafazzin recapitulates all of the phospholipid abnormalities observed in human patients and many of the mitochondrial defects. Another major project in our lab focuses on the mitochondrial ADP/ATP carrier that is required for oxidative phosphorylation. Researchers are studying how these novel interactions help establish normal mitochondrial function, the biochemical details of these associations, and whether disturbances in these assemblies can contribute to mitochondrial dysfunction.
Research Summary
Phospholipids are the building blocks of biological membranes. Membranes leverage the amphipathic chemistry of lipids to form bilayers that encapsulate a cell and its multitude of organelles. Such compartmentalization has enabled cells to separate biochemical pathways, establish specialized functions that can respond when appropriate, and adapt to constantly fluctuating metabolic conditions. The Claypool laboratory’s research focus is on the underappreciated contribution of the mitochondrion to cellular phospholipid metabolism. In addition to being the sole producer of the canonical mitochondrial lipid, cardiolipin (CL), the mitochondrion hosts one of the two major pathways in a cell for the production of phosphatidylethanolamine (PE). PS decarboxylase 1 (Psd1) is an integral inner mitochondrial membrane protein that produces the vast majority of PE in the mitochondrion and can provide the entire cellular complement of PE in yeast. Ablation of the mitochondrial capacity to synthesize either CL or PE is embryonically lethal in mice. The mitochondrial pathway of PE production therefore provides a pool of this lipid that cannot be replaced by the other three PE biosynthetic pathways. Thus, both CL and PE are crucial for mammalian development and have distinct and yet overlapping properties that are essential not only for mitochondrial function, but life itself.
Ongoing projects are focused on defining how lipids and membrane proteins interact to establish and maintain normal mitochondrial function and how derangements in this complex relationship result in pathophysiology.
PubMed
https://www.ncbi.nlm.nih.gov/myncbi/browse/collection/41156711/?sort=date&direction=descending
Selected Publications
Baile MG and Claypool SM. “The power of yeast to model diseases of the powerhouse of the cell.” Front Biosci. 2013 Jan 1;18:241-78.
Baile MG, Whited K, Claypool SM. “Deacylation on the matrix side of the mitochondrial inner membrane regulates cardiolipin remodeling.” Mol Biol Cell. 2013 Jun;24(12):2008-20
Claypool SM and Koehler CM. “The Complexity of Cardiolipin in Health and Disease.” Trends Biochem Sci. 2012 Jan;37(1): 32-41.
Claypool SM, Whited K, Srijumnong S, Han X, Koehler CM. “Barth syndrome mutations that cause tafazzin complex lability.” J Cell Biol. 2011 Feb 7;192(3):447-62
Tamura Y, Onguka O, Hobbs AE, Jensen RE, Iijima M, Claypool SM, Sesaki H. “Role for two conserved intermembrane space proteins, Ups1p and Up2p, in intra-mitochondrial phospholipid trafficking.” J Biol Chem. 2012 May 4;287(19):15205-18
Tamura Y, Onguka O, Itoh K, Endo T, Iijima M, Claypool SM, Sesaki H. “Phosphatidylethanolamine biosynthesis in mitochondria: phosphatidylserine (PS) trafficking is independent of a PS decarboxylase and intermembrane space proteins, Ups1p and Ups2p.” J Biol Chem. 2012 Dec 21;287(52):43961-71
Whited K, Baile MG, Currier P, Claypool SM. “Seven functional classes of Barth syndrome mutation.” Hum Mol Genet. 2013 Feb 1; 22(3): 483-492.
Honors
- UCLA Postdoctoral Recognition Award, Certificate of Excellence, 1/1/07
- NIH Pathway to Independence Award, NHLBI, 1/1/07
- Postdoctoral Fellowship Award, Research Committee of the American Heart Association (AHA), 1/1/04
Memberships
- American Society for Biochemistry and Molecular Biology, Member
- American Society of Cell Biology, Member
Additional Training
University of California, Los Angeles, Los Angeles, CA, 2008, Mitochondrial Biology