Modelling a pathological GSX2 variant that selectively alters DNA binding reveals hypomorphic mouse brain defects.

Gsx2 is a homeodomain transcription factor critical for development of the ventral telencephalon and hindbrain in mouse. Loss of Gsx2 function results in severe basal ganglia dysgenesis and defects in the nucleus tractus solitarius (nTS) of the hindbrain, together with respiratory failure at birth. De Mori et al.