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Deprecated: Implicit conversion from float 336.4 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Biol+Chem 2014 ; 289 (17): 11816-11828 Nephropedia Template TP
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Reactive oxygen species, AMP-activated protein kinase, and the transcription cofactor p300 regulate alpha-tubulin acetyltransferase-1 (alphaTAT-1/MEC-17)-dependent microtubule hyperacetylation during cell stress #MMPMID24619423
Mackeh R; Lorin S; Ratier A; Mejdoubi-Charef N; Baillet A; Bruneel A; Hamai A; Codogno P; Pous C; Perdiz D
J Biol Chem 2014[Apr]; 289 (17): 11816-11828 PMID24619423show ga
Beyond its presence in stable microtubules, tubulin acetylation can be boosted after UV exposure or after nutrient deprivation, but the mechanisms of microtubule hyperacetylation are still unknown. In this study, we show that this hyperacetylation is a common response to several cellular stresses that involves the stimulation of the major tubulin acetyltransferase MEC-17. We also demonstrate that the acetyltransferase p300 negatively regulates MEC-17 expression and is sequestered on microtubules upon stress. We further show that reactive oxygen species of mitochondrial origin are required for microtubule hyperacetylation by activating the AMP kinase, which in turn mediates MEC-17 phosphorylation upon stress. Finally, we show that preventing microtubule hyperacetylation by knocking down MEC-17 affects cell survival under stress conditions and starvation-induced autophagy, thereby pointing out the importance of this rapid modification as a broad cell response to stress.