Loss of intermediate filament IFB-1 reduces mobility, density, and physiological function of mitochondria in Caenorhabditis elegans sensory neurons.

Autor: Barmaver SN; Department of Life Science, National Tsing Hua University, Institute of Molecular and Cellular Biology, Hsinchu, Taiwan., Muthaiyan Shanmugam M; Department of Life Science, National Tsing Hua University, Institute of Molecular and Cellular Biology, Hsinchu, Taiwan., Chang Y; Department of Life Science, National Tsing Hua University, Institute of Molecular and Cellular Biology, Hsinchu, Taiwan., Bayansan O; Department of Life Science, National Tsing Hua University, Institute of Molecular and Cellular Biology, Hsinchu, Taiwan., Bhan P; Department of Life Science, National Tsing Hua University, Institute of Molecular and Cellular Biology, Hsinchu, Taiwan.; Research Center for Healthy Aging, China Medical University, Taichung, Taiwan., Wu GH; Department of Life Science, National Tsing Hua University, Institute of Molecular and Cellular Biology, Hsinchu, Taiwan., Wagner OI; Department of Life Science, National Tsing Hua University, Institute of Molecular and Cellular Biology, Hsinchu, Taiwan.
Jazyk: angličtina
Zdroj: Traffic (Copenhagen, Denmark) [Traffic] 2022 May; Vol. 23 (5), pp. 270-286. Date of Electronic Publication: 2022 Mar 16.
DOI: 10.1111/tra.12838
Abstrakt: Mitochondria and intermediate filament (IF) accumulations often occur during imbalanced axonal transport leading to various types of neurological diseases. It is still poorly understood whether a link between neuronal IFs and mitochondrial mobility exist. In Caenorhabditis elegans, among the 11 cytoplasmic IF family proteins, IFB-1 is of particular interest as it is expressed in a subset of sensory neurons. Depletion of IFB-1 leads to mild dye-filling and significant chemotaxis defects as well as reduced life span. Sensory neuron development is affected and mitochondrial transport is slowed down leading to reduced densities of these organelles. Mitochondria tend to cluster in neurons of IFB-1 mutants likely independent of the fission and fusion machinery. Oxygen consumption and mitochondrial membrane potential is measurably reduced in worms carrying mutations in the ifb-1 gene. Membrane potential also seems to play a role in transport such as carbonyl cyanide p-(trifluoromethoxy)phenylhydrazone treatment led to increased directional switching of mitochondria. Mitochondria co-localize with IFB-1 in worm neurons and appear in a complex with IFB-1 in pull-down assays. In summary, we propose a model in which neuronal IFs may serve as critical (transient) anchor points for mitochondria during their long-range transport in neurons for steady and balanced transport.
(© 2022 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
Databáze: MEDLINE
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