Posttranslational modifications play crucial roles in synaptic plasticity and memory formation. The important role of histone acetylation is well established in these processes. However, activity-dependent regulation of acetylation of non-histone proteins is not well understood. We previously showed that α-tubulin is acetylated in an activity-dependent manner. Here, we show that cyclin-dependent kinase 5 (CDK5) plays an important role in α-tubulin acetylation induced by KCl depolarization or N-methyl-D-aspartate stimulation of the hippocampal slices. In addition, KCl depolarization inhibits the activity of SIRT2, an α-tubulin deacetylase. The inhibitory effect of KCl on SIRT2 activity requires CDK5 activity. Furthermore, α-tubulin acetylation is enhanced by memory training in object recognition task. These results suggest that memory formation may involve α-tubulin acetylation.

中文翻译：

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活动和记忆训练诱导海马中α-微管蛋白的乙酰化。

翻译后修饰在突触可塑性和记忆形成中起关键作用。在这些过程中，组蛋白乙酰化的重要作用已得到充分确立。然而，非组蛋白的乙酰化的活性依赖调节尚不十分清楚。我们以前表明，α-微管蛋白以活性依赖性方式被乙酰化。在这里，我们显示细胞周期蛋白依赖性激酶5（CDK5）在由KCl去极化或海马切片N-甲基-D-天冬氨酸刺激诱导的α-微管蛋白乙酰化中起重要作用。另外，KCl去极化抑制了α-微管蛋白脱乙酰基酶SIRT2的活性。KCl对SIRT2活性的抑制作用需要CDK5活性。此外，在对象识别任务中通过记忆训练增强了α-微管蛋白的乙酰化。