Atat1, short for α -tubulin acetyltransferase 1, is an enzyme responsible for the acetylation of α -tubulin on lysine 40. This post -translational modification is linked to the presence of long -lived stable microtubules, which are more resistant to mechanical breakdown. The acetylation process by Atat1 modulates microtubule dynamics and is involved in multiple cellular activities such as cell motility, mitosis, cytoskeletal organization, and intracellular trafficking [1].

In Atat1 knockout mouse models, starting at postnatal day 5, mutant mice display enlarged lateral ventricles in the forebrain due to hypoplasia in the septum and striatum, resembling human ventriculomegaly. Behavioral tests also show deficits in motor coordination, indicating that Atat1 is crucial for forebrain development [2]. Additionally, in microglia/macrophage cells, silencing Atat1 enhances erythrophagocytosis. In Atat1 -/-mice, there is increased phagocytosis of red blood cells in the peri -hematoma and reduced hematoma volume after intracerebral hemorrhage, along with improved neurological recovery [3].

In conclusion, Atat1 is essential for regulating microtubule acetylation and is involved in various biological processes. The study of Atat1 knockout mouse models has revealed its significance in forebrain development and in processes related to intracerebral hemorrhage, providing insights into potential therapeutic targets for related diseases.