MOV10, an RNA helicase, is a significant player in the cellular RNA metabolism. It associates with the RNA-induced silencing complex component Argonaute (AGO), likely resolving RNA secondary structures. It is also involved in the nonsense-mediated RNA decay pathway through its association with UPF1 [1]. MOV10 is widely expressed and plays a crucial role in the cellular response to viral infection, suppression of retrotransposition, and development [1].

Knockout of Mov10 leads to embryonic lethality, highlighting its essential role in development, specifically for the completion of gastrulation [1]. In the testes, knockdown of Mov10 disrupts the proliferation of spermatogonial progenitor cells [1]. In the brain, MOV10 is elevated postnatally, binds mRNAs encoding cytoskeleton and neuron projection proteins, and is important for neuronal architecture [1]. Heterozygous Mov10 mutant mice are hyperactive and anxious, and their cultured hippocampal neurons have reduced dendritic arborization [1]. Zygotic knockdown of Mov10 in Xenopus laevis causes abnormal head and eye development and mislocalization of neuronal precursors in the brain [1]. Additionally, in mice, MOV10 restricts LINE1 retrotransposition in a dosage-dependent manner [2].

In conclusion, MOV10 is vital for normal development, especially during gastrulation, and has key functions in neuronal development and function. It also plays a significant role in protecting the host from viral infections and controlling retrotransposition. The use of gene knockout models, such as in mice and Xenopus laevis, has been instrumental in revealing these functions, which are relevant to understanding embryonic development, neuronal-related disorders, and viral-host interactions.