Glancy 2015 Nature: Difference between revisions

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|year=2015
|year=2015
|journal=Nature
|journal=Nature
|abstract=Intracellular energy distribution has attracted much interest and has been proposed to occur in skeletal muscle via metabolite-facilitated diffusion [1,2]
|abstract=Intracellular energy distribution has attracted much interest and has been proposed to occur in skeletal muscle via metabolite-facilitated diffusion [1,2]; however, genetic evidence suggests that facilitated diffusion is not critical for normal function [3โ€“7]. We hypothesized that mitochondrial structure minimizes metabolite diffusion distances in skeletal muscle. Here we demonstrate a mitochondrial reticulum providing a conductive pathway for energy distribution, in the form of the proton-motive force, throughout the mouse skeletal muscle cell. Within this reticulum, we find proteins associated with mitochondrial proton-motive force production preferentially in the cell periphery and proteins that use the proton-motive force for ATP production in the cell interior near contractile and transport ATPases. Furthermore, we show a rapid, coordinated depolarization of the membrane potential component of the proton-motive force throughout the cell in response to spatially controlled uncoupling of the cell interior. We propose that membrane potential conduction via the mitochondrial reticulum is the dominant pathway for skeletal muscle energy distribution.
; however, genetic evidence suggests that facilitated diffusion is not critical for normal function [3โ€“7]. We hypothesized that mitochondrial structure minimizes metabolite diffusion distances in skeletal muscle. Here we demonstrate a mitochondrial reticulum providing a conductive pathway for energy distribution, in the form of the proton-motive force, throughout
the mouse skeletal muscle cell. Within this reticulum, we find proteins associated with mitochondrial proton-motive force production preferentially in the cell periphery and proteins that use the
proton-motive force for ATP production in the cell interior near
contractile and transport ATPases. Furthermore, we show a rapid,
coordinated depolarization of the membrane potential component
of the proton-motive force throughout the cell in response to spatially controlled uncoupling of the cell interior. We propose that
membrane potential conduction via the mitochondrial reticulum
is the dominant pathway for skeletal muscle energy distribution.
}}
}}
{{Labeling
{{Labeling

Revision as of 11:03, 30 July 2015

Publications in the MiPMap
Glancy B, Hartnell LM, Malide D, Yu ZX , Combs CA, Connelly PS, Subramaniam S, Balaban RS (2015) Mitochondrial reticulum for cellular energy distribution in muscle. Nature 523:617-23.

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Glancy B, Hartnell LM, Malide D, Yu ZX, Combs CA, Connelly PS, Subramaniam S, Balaban RS (2015) Nature

Abstract: Intracellular energy distribution has attracted much interest and has been proposed to occur in skeletal muscle via metabolite-facilitated diffusion [1,2]; however, genetic evidence suggests that facilitated diffusion is not critical for normal function [3โ€“7]. We hypothesized that mitochondrial structure minimizes metabolite diffusion distances in skeletal muscle. Here we demonstrate a mitochondrial reticulum providing a conductive pathway for energy distribution, in the form of the proton-motive force, throughout the mouse skeletal muscle cell. Within this reticulum, we find proteins associated with mitochondrial proton-motive force production preferentially in the cell periphery and proteins that use the proton-motive force for ATP production in the cell interior near contractile and transport ATPases. Furthermore, we show a rapid, coordinated depolarization of the membrane potential component of the proton-motive force throughout the cell in response to spatially controlled uncoupling of the cell interior. We propose that membrane potential conduction via the mitochondrial reticulum is the dominant pathway for skeletal muscle energy distribution.


Labels: MiParea: mt-Membrane 


Organism: Mouse  Tissue;cell: Skeletal muscle 




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