Tuesday, October 20, 2020
Mitochondrial Health

Jared Rutter (U. Utah, HHMI) 2: Mitochondrial Metabolism and Cell Decisions



https://www.ibiology.org/cell-biology/mitochondria-metabolism

Dr. Jared Rutter shares new insights into the interplay between mitochondria, metabolism, and cellular behavior.

Mitochondria are integral to the metabolism of eukaryotic cells, yet many of their properties are not fully understood. In Part 1 of this iBioSeminar, Dr. Jared Rutter lays out the foundational knowledge of mitochondrial structure and origin, and shares what is currently known about mitochondrial roles in metabolism, protein homeostasis, and signaling. He ends by highlighting a focus of his research group: to unravel the functions of uncharacterized mitochondrial proteins.

In Part 2 of his talk, Rutter describes his group’s work to unravel the relationship between the activity of the Mitochondrial Pyruvate Carrier (MPC) and the behavior of numerous cell types, including cancer and stem cells. His group found that forced expression of the MPC in multiple stem cell models led to reduced “stemness” and proliferative capacity, and that MPC inhibition could promote organoid formation in culture and tumor formation in vivo. These data indicate an important link between mitochondria, metabolism, and cell behavior.

In his Part 3, Rutter emphasizes the challenge of mitochondrial protein synthesis. How do the components of the electron transport chain (ETC) assemble in the right stoichiometry at the right time? Rutter introduces the LYR family of proteins, which aid assembly of ETC components. LYR proteins interact with a common binding partner, the acyl carrier protein (ACP), via a unique fatty acyl moiety on ACP. Rutter’s group showed that ACP acylation is necessary for assembly of the ETC and activation of oxidative phosphorylation.

Speaker Biography:
Jared Rutter is a Professor of Biochemistry and holds the Dee Glen and Ida Smith Endowed Chair for Cancer Research at the University of Utah. Dr. Rutter received his PhD from the University of Texas Southwestern Medical Center in 2001, working with Dr. Steve McKnight. After receiving his PhD, he spent 18 months as the Sara and Frank McKnight Independent Fellow of Biochemistry before joining the faculty at the University of Utah. As of September 2015, Dr. Rutter is an Investigator of the Howard Hughes Medical Institute. In addition to leading his laboratory at the University of Utah, Dr. Rutter is also actively involved in translating these academic discoveries into therapies as a founder, consultant and board member of several companies and venture firms. Dr. Rutter also serves as co-Director of the Diabetes and Metabolism Center at the University of Utah and co-Leader of the Nuclear Control of Cell Growth and Differentiation at Huntsman Cancer Institute.

https://rutter.biochem.utah.edu

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18 thoughts on “Jared Rutter (U. Utah, HHMI) 2: Mitochondrial Metabolism and Cell Decisions
  1. I wonder if mct4 is inhibited thus reverse lactate and pushes Pyruvate down if this process then downgrades mtor?
    How does this pathway change in ketosis using ketones instead of glucose?
    Does fasting thus mitophagy allow for better function of MPC or is the lack of two proteins needed constant?
    Can we measure mct4? To assume more cell growth ie cancer?

  2. Don't know if it's a good thing or a bad thing…. but MitoQ has a mitochondrial absorption rate that boggles the mind. Some people who have taken it have had astounding improvements in their health conditions.

  3. This is phenomenal work. It reminded me of some work being done by Dr. Inigo San Millan at University of Colorado on mitochondrial dysfunction as a person drifts from insulin resistance to T2DM. I wonder if there is an obvious crossover in the MPC and MCT4 effects as Dr. Milian found out from muscle biopsies that the muscle cells of people with insulin resistance started to exclusively use glycolosis for energy production rather than burning fatty acids in the mitochondria (i.e. the mitochondria weren't being used for energy production at all). This change resulted in higher lactate levels plus the health issues that are all too familiar these days. Dr. Milian discussed his work in detail in a Peter Attia podcast and at a lower level in this paper. https://www.endocrineweb.com/professional/metabolic-syndrome/jumpstarting-weight-loss-patients-metabolic-disease

  4. Fascinating! But consider evolution: 3:25 "There's an MPC1 protein and an MPC2 protein. Those two proteins come together. Both of them are absolutely required for the function of this complex. And in the absence of one or the other, the other one just gets degraded."

    Which one of these proteins originally evolved first? And wouldn't the tenets of natural selection be violated when that organism selected and preserved that useless first protein for eons of generations before the second one evolved?

  5. Thanks for the great work and the presentations. I hope your therapeutic venture is successful. A friendly suggestion–stop using the word, allude! You are using it incorrectly, and too often! Degrades the appearance of competence that your work deserves.

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