Lack of myosin VI in adult mice led to brain enlargement and increased GFAP levels, indicating a role in brain maturation and age-dependent gliosis.
Lack of unconventional myosin VI in mice leads to age-dependent brain enlargement and development of profound gliosis.
Absolute Event Rate: 0% vs 0%
Myosin VI (MVI) is a unique unconventional myosin which, unlike other myosins, moves towards the minus end of actin filaments. It is involved in numerous cellular processes such as endocytosis and trafficking, cell migration and adhesion, and gene transcription. It is widely expressed in all tissues, including the brain. Its lack in adult murine brains is associated with gliosis and impairment of neuronal transmission. Here, we demonstrate that the MVI level in the total mouse brain and its regions (cerebral cortex, cerebellum, and hippocampus) increases with the animal’s age (from newborn up to 12‑month‑old mice). Its lack leads to enlargement of the brain and its examined areas, and an increase of the level of GFAP, the marker of glia cells, in adult mice. The data indicate an involvement of MVI in the brain maturation and possibly in development of an age‑dependent gliosis.
Nowak et al. (Sat,) reported a other. Lack of myosin VI in adult mice led to brain enlargement and increased GFAP levels, indicating a role in brain maturation and age-dependent gliosis.