ATAT1-enriched vesicles promote microtubule acetylation via axonal transport

Aviel Even; Giovanni Morelli; Loïc Broix; Chiara Scaramuzzino; Silvia Turchetto; Ivan Enghian Gladwyn-Ng; Romain Le Bail; Michal Shilian; Stephen D. Freeman; Maria M. Magiera; A. S. Jijumon; Nathalie Krusy; Brigitte Malgrange; Bert Brône; Paula Dietrich; Ioannis Dragatsis; Carsten Janke; Frédéric Saudou; Miguel Weil; Laurent Nguyen

doi:10.1126/sciadv.aax2705

NeuroscienceScience AdvancesDec 6, 2019

Peer-reviewed journal article

ATAT1-enriched vesicles promote microtubule acetylation via axonal transport

Aviel Even iD, Giovanni Morelli iD, Loïc Broix iD, Chiara Scaramuzzino iD, Silvia Turchetto iD, Ivan Enghian Gladwyn-Ng iD, Romain Le Bail iD, Michal Shilian iD, Stephen D. Freeman iD, Maria M. Magiera iD, A. S. Jijumon iD, Nathalie Krusy, Brigitte Malgrange iD, Bert Brône iD, Paula Dietrich iD, Ioannis Dragatsis iD, Carsten Janke iD, Frédéric Saudou iD, Miguel Weil iD, Laurent Nguyen iD

Abstract

Microtubules are polymerized dimers of - and {beta}-tubulin that underlie a broad range of cellular activities. Acetylation of -tubulin by the acetyl-transferase ATAT1 modulates microtubule dynamics and functions in neurons. However, it remains unclear how and why this enzyme acetylates microtubules over long distances in axons. Here, we show that loss of ATAT1 impairs axonal transport in neurons and cell free motility assays confirm a requirement of tubulin acetylation for proper bidirectional vesicular transport. Moreover, we demonstrate that the main cellular pool of ATAT1 is transported at the cytosolic side of neuronal vesicles that are moving along axons. Altogether, our data suggest that axonal transport of ATAT1-enriched vesicles is the predominant driver of -tubulin acetylation in axons.

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