Hosseini Shirin, van Ham Marco, Erck Christian, Korte Martin, Michaelsen-Preusse Kristin
Department of Cellular Neurobiology, Zoological Institute, Technische Universität Braunschweig, Braunschweig, Germany.
Research Group Neuroinflammation and Neurodegeneration, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Front Mol Neurosci. 2022 Oct 19;15:931859. doi: 10.3389/fnmol.2022.931859. eCollection 2022.
Microtubules (MTs) are central components of the neuronal cytoskeleton and play a critical role in CNS integrity, function, and plasticity. Neuronal MTs are diverse due to extensive post-translational modifications (PTMs), particularly detyrosination/tyrosination, in which the C-terminal tyrosine of α-tubulin is cyclically removed by a carboxypeptidase and reattached by a tubulin-tyrosine ligase (TTL). The detyrosination/tyrosination cycle of MTs has been shown to be an important regulator of MT dynamics in neurons. TTL-null mice exhibit impaired neuronal organization and die immediately after birth, indicating TTL function is vital to the CNS. However, the detailed cellular role of TTL during development and in the adult brain remains elusive. Here, we demonstrate that conditional deletion of TTL in the neocortex and hippocampus during network development results in a pathophysiological phenotype defined by incomplete development of the corpus callosum and anterior commissures due to axonal growth arrest. TTL loss was also associated with a deficit in spatial learning, impaired synaptic plasticity, and reduced number of spines in hippocampal neurons, suggesting that TTL also plays a critical role in hippocampal network development. TTL deletion after postnatal development, specifically in the hippocampus and in cultured hippocampal neurons, led to a loss of spines and impaired spine structural plasticity. This indicates a novel and important function of TTL for synaptic plasticity in the adult brain. In conclusion, this study reveals the importance of α-tubulin tyrosination, which defines the dynamics of MTs, in controlling proper network formation and suggests TTL-mediated tyrosination as a new key determinant of synaptic plasticity in the adult brain.
微管(MTs)是神经元细胞骨架的核心组成部分,在中枢神经系统(CNS)的完整性、功能和可塑性方面发挥着关键作用。由于广泛的翻译后修饰(PTMs),特别是去酪氨酸化/酪氨酸化,神经元微管具有多样性,其中α-微管蛋白的C末端酪氨酸被羧肽酶循环去除,并由微管蛋白-酪氨酸连接酶(TTL)重新连接。微管的去酪氨酸化/酪氨酸化循环已被证明是神经元中微管动力学的重要调节因子。TTL基因敲除小鼠表现出神经元组织受损,并在出生后立即死亡,这表明TTL功能对中枢神经系统至关重要。然而,TTL在发育过程中和成年大脑中的详细细胞作用仍不清楚。在这里,我们证明在网络发育期间新皮层和海马体中TTL的条件性缺失会导致一种病理生理表型,其特征是由于轴突生长停滞导致胼胝体和前连合发育不完全。TTL缺失还与空间学习缺陷、突触可塑性受损以及海马神经元棘突数量减少有关,这表明TTL在海马网络发育中也起着关键作用。出生后发育后,特别是在海马体和培养的海马神经元中删除TTL,会导致棘突丢失和棘突结构可塑性受损。这表明TTL在成年大脑的突触可塑性中具有新的重要功能。总之,这项研究揭示了定义微管动力学的α-微管蛋白酪氨酸化在控制正确网络形成中的重要性,并表明TTL介导的酪氨酸化是成年大脑突触可塑性的一个新的关键决定因素。