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Fueled by microtubules: Does tubulin dimer/polymer partitioning regulate intracellular metabolism?
Author(s) -
Cassimeris Lynne,
Silva Victoria Caruso,
Miller Elizabeth,
Ton Quynh,
Molnar Cody,
Fong John
Publication year - 2012
Publication title -
cytoskeleton
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.95
H-Index - 86
eISSN - 1949-3592
pISSN - 1949-3584
DOI - 10.1002/cm.21008
Subject(s) - tubulin , microtubule , biology , intracellular , microbiology and biotechnology , biochemistry , dimer , transporter , signal transduction , biophysics , chemistry , gene , organic chemistry
Microtubules (MTs) or their subunits, tubulin dimers, interact with multiple components that contribute to intracellular metabolic pathways. MTs are required for insulin‐dependent transport of glucose transporter 4 to the plasma membrane, they bind most glycolytic enzymes and are required for translation of the mRNA encoding hypoxia inducible factor‐1α. Tubulin dimers bind the voltage‐dependent anion channel of the mitochondrial outer membrane; this channel functions in metabolite transport in and out of mitochondria. We hypothesize that tubulin partitioning between dimer and polymer pools regulates multiple steps in metabolism, where metabolic output is greatest when both tubulin dimers and MT polymers are present and reduced by drug treatments that disrupt this normal balance. Experimental evidence from these drug‐induced changes in tubulin dimer/polymer partitioning supports our model for several metabolic steps. Signal transduction pathways that stabilize or destabilize MTs can shift the normal ratio between unpolymerized and polymerized tubulin dimers, and one downstream consequence of this shift in tubulin partitioning could be a change in metabolic output. © 2012 Wiley Periodicals, Inc

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