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Hiromi Sesaki, Ph.D.

Photo of Dr. Hiromi Sesaki, Ph.D.
  • Professor of Cell Biology

Research Interests

Membrane fusion and fission; Mitochondrial dynamics

Background

Dr. Hiromi Sesaki is an associate 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.

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Titles

  • Professor of Cell Biology

Departments / Divisions

Centers & Institutes

Education

Degrees

  • Ph.D., Osaka University (Japan) (1997)
  • B.S., Osaka University (Japan) (1990)

Additional Training

Johns Hopkins University, Baltimore, MD, 2002, Cell Biology

Research & Publications

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

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

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

Tamura Y, Itoh K, and Sesaki H. (2011). SnapShot: Mitochondrial dynamics. Cell. 145:1158-11581e

Cerveny, K.L., Studer, S.L., Jensen, R.E., and Sesaki, H. (2007). Yeast mitochondrial division and distribution requires the cortical Num1 protein. Dev. Cell. 12: 363-375

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

Academic Affiliations & Courses

Graduate Program Affiliation

Biochemistry, Cellular and Molecular Biology Graduate Program

Activities & Honors

Memberships

  • Mitochondrion
    Editorial Board
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