α-Tubulin Acetyltransferase Is a Novel Target Mediating Neurite Growth Inhibitory Effects of Chondroitin Sulfate Proteoglycans and Myelin-Associated Glycoprotein

ENeuro
Victor S C WongBrett Langley

Abstract

Damage to the CNS results in neuronal and axonal degeneration, and subsequent neurological dysfunction. Endogenous repair in the CNS is impeded by inhibitory chemical and physical barriers, such as chondroitin sulfate proteoglycans (CSPGs) and myelin-associated glycoprotein (MAG), which prevent axon regeneration. Previously, it has been demonstrated that the inhibition of axonal histone deacetylase-6 (HDAC6) can promote microtubule α-tubulin acetylation and restore the growth of CSPGs- and MAG-inhibited axons. Since the acetylation of α-tubulin is regulated by two opposing enzymes, HDAC6 (deacetylation) and α-tubulin acetyltransferase-1 (αTAT1; acetylation), we have investigated the regulation of these enzymes downstream of a growth inhibitory signal. Our findings show that exposure of primary mouse cortical neurons to soluble CSPGs and MAG substrates cause an acute and RhoA-kinase-dependent reduction in α-tubulin acetylation and αTAT1 protein levels, without changes to either HDAC6 levels or HDAC6 activity. The CSPGs- and MAG-induced reduction in αTAT1 occurs primarily in the distal and middle regions of neurites and reconstitution of αTAT1, either by Rho-associated kinase (ROCK) inhibition or lentiviral-mediated αTAT1 overexp...Continue Reading

Citations

May 24, 2019·The Journal of Cell Biology·Ludo Van Den Bosch
May 10, 2019·The Journal of Cell Biology·Ashley L KalinskiJeffery L Twiss
Jul 28, 2018·Frontiers in Cellular Neuroscience·Anna RonowskaAgnieszka Jankowska-Kulawy
Jul 28, 2020·Frontiers in Cellular Neuroscience·Armin SamiShuxin Li
Dec 17, 2020·Developmental Neurobiology·Marie-Jo MoutinAnnie Andrieux

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Methods Mentioned

BETA
acetylation
Assay
protein assay
PCRs
GTPase

Software Mentioned

ImageJ

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