Hiromi Sesaki, PhD
Highlights
Languages
- English
Gender
MaleJohns Hopkins Affiliations:
- Johns Hopkins School of Medicine Faculty
About Hiromi Sesaki
Primary Academic Title
Professor of Cell Biology
Background
Dr. Hiromi Sesaki is a professor of cell biology at the Johns Hopkins University School of Medicine. His research explores the molecular mechanisms and physiological roles of mitochondrial fusion and division.
Dr. Sesaki received his B.S. in biology and Ph.D. in physiology, both from Osaka University in Japan. He completed a postdoctoral fellowship in cell biology at Johns Hopkins. He joined the Johns Hopkins faculty in 2006.
He has authored or co-authored more than 100 peer-reviewed publications and two book chapters, and serves on the editorial board of the journal Mitochondrion. His research has garnered several awards and NIH grants.
Centers and Institutes
Research Interests
Membrane fusion and fission, Mitochondrial dynamics
Lab Website
Iijima & Sesaki - Lab Website
Research Summary
The Sesaki laboratory is interested in the molecular mechanisms and physiological roles of mitochondrial fusion and division. Mitochondria are highly dynamic and control their morphology by a balance of fusion and division. The regulation of membrane fusion and division generates a striking diversity of mitochondrial shapes, ranging from numerous small spheres in hepatocytes to long branched tubules in myotubes. In addition to shape and number, mitochondrial fusion is critical for normal organelle function. For example, mice that are defective in mitochondrial fusion die during early development while yeast fusion mutants rapidly lose their mitochondria genome and become incapable of oxidative phosphorylation. Moreover, mitochondrial fusion also regulates the release of cytochrome C during apoptosis. Therefore, it is not surprising that defects in mitochondrial fusion cause neurodegenerative disorders in humans, including Charcot-Marie-Tooth disease type 2A and autosomal dominant optic atrophy.
Using yeast as a model system, the lab has identified several components that mediate and regulate mitochondrial fusion. The lab is currently trying to determine their functions in both yeast and mammals. The goals of this research are to understand the molecular basis of mitochondrial fusion and division using biochemical approaches and to determine the physiological roles of mitochondrial fusion using cell culture and animal models.
Selected Publications
Adachi, Y., Kato, T., Yamada, T., Murata, D., Arai, K., Stahelin, R.V., Chan, D.C., Iijima, M., and Sesaki, H. (2020). Mol Cell. 80: 621-632
Adachi Y, Itoh K, Yamada T, Cerveny KL, Suzuki TL, Macdonald P, Frohman MA, Ramachandran R, Iijima M, and Sesaki H. (2016) Coincident phosphatidic acid interaction restrains Drp1 in mitochondrial division. Mol. Cell. 63: 1034-43
Senoo H, Kamimura K, Kimura R, Nakajima A, Sawai S, Sesaki H, Iijima M. (2019). Phosphorylated Rho-GDP directly activates mTORC2 Kinase toward AKT through dimerization with Ras-GTP to regulate cell migration. Nat. Cell Biol. 21: 867-878
Tamura Y, Itoh K, and Sesaki H. (2011). SnapShot: Mitochondrial dynamics. Cell. 145:1158-11581e
Yamada T, Murata D, Adachi Y, Itoh K, Kameoka S, Igarashi A, Kato T, Araki Y, Huganir RL, Dawson TM, Yanagawa T, Okamoto K, Iijima M, Sesaki H. (2018). Mitochondrial stasis reveals p62-mediated ubiquitination in parkin-independent mitophagy and mitigates nonalcoholic fatty liver disease. Cell Metab. 28: 588-604
Graduate Program Affiliations
Biochemistry, Cellular and Molecular Biology Graduate Program
Memberships
- Mitochondrion, Editorial Board