Vti1a, short for Vesicle transport through interaction with t-SNAREs 1A, is a member of the N-ethylmaleimide-sensitive factor attachment protein receptor protein family. It functions as a vesicular protein involved in cell signaling and mediates vesicle trafficking. This process is crucial for many biological pathways, especially those related to neuronal function, development, and autophagy [1,3]. Genetic models, such as knockout (KO) mouse models, have been instrumental in understanding its functions.

In KO mouse models, the loss of Vti1a and Vti1b leads to death at birth with massive neurodegeneration in peripheral ganglia and defective axon tracts [2]. In neurons lacking Vti1a and Vti1b, there are significant alterations in neuronal development, including shorter neurite lengths and absence of Golgi outposts in dendrites [2]. Vti1a/b-deficient neurons also show severe impairment in synaptic vesicle and dense-core vesicle secretion, with reduced levels of secretion-mediating proteins at synapses [4]. Additionally, ablation of Vti1a/1b in mouse cortex triggers neural progenitor pool depletion and cortical layer 5 malformation [5].

In conclusion, Vti1a is essential for neuronal development, synaptic vesicle and dense-core vesicle secretion, and neural progenitor maintenance. Studies using KO mouse models have revealed its significance in these biological processes. Dysfunction of Vti1a may be associated with nervous system disorders, such as hepatic encephalopathy, amyotrophic lateral sclerosis, and glioma, highlighting its importance in understanding disease mechanisms [1].