Otx2, which is an encoded protein that plays the role of a transcription factor, has also been shown to be involved in the regional patterning of the midbrain and forebrain.

Otx2 mutations have also been associated with seizures, developmental delays, short stature, structural abnormalities of the pituitary gland, and an early onset of degeneration of the retina.

In the mouse, studies have shown development of the retina is regulated in a cell type- and stage-specific manner by seven Otx2 cis-regulatory modules.

[7] A “knockin” mouse line was generated where Crx (Otx family homeoprotein) was replaced by Otx2 and vice versa to examine the functional substitutability.

[9] Otx2 is expressed in the brain, ear, nose and eye, and in the case of mutations; it can lead to significant developmental abnormalities and disorders.

[14] Dark-rearing from birth and binocular enucleation of rats resulted in decreased expression of PV-cells and Otx2, which suggests that these proteins are visually experience-driven.

At the molecular level, Otx2 induction partially compensates the gene expression changes induced by Nanog overexpression in the absence of LIF.

Ethanol consumption during embryogenesis, leads to a reduction in Otx2 mRNA in the central nervous system altering gene expression.

In order to detect if the reduction of Otx2 due to ethanol caused an increase in binge-drinking behaviors in adults, a lentiviral hairpin (sh)RNA was used to target Otx2 and reduce the levels of Otx2 expression in the VTA in mice.

Binge-like ethanol drinking increases otx2, wnt1, and mdk gene expression in the ventral tegmental area of adult mice.

Neuroscience Insights, 16, 263310552110098. https://doi.org/10.1177/26331055211009850 == External links == This article incorporates text from the United States National Library of Medicine, which is in the public domain.