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Studies proposed a model for embryonic neurogenesis where the expression levels of the SOXB2 and SOXB1 factors regulate the differentiation status of the neural stem cells. However, the precise role of the SOXB2 genes remains controversial. Therefore, this study aims to investigate the effects of individual deletions of the  SOX21  and  SOX14  genes during the development of the dorsal midbrain. We show that SOX21 and SOX14 function distinctly during the commitment of the GABAergic lineage. More explicitly, deletion of  SOX21  reduced the expression of the GABAergic precursor marker GATA3 and BHLHB5 while the expression of GAD6, which marks GABAergic terminal differentiation, was not affected. In contrast deletion of  SOX14  alone was sufficient to inhibit terminal differentiation of the dorsal midbrain GABAergic neurons. Furthermore, we demonstrate through gain-of-function experiments, that despite the homology of  SOX21  and  SOX14 , they have unique gene targets and cannot compensate for the loss of each other. Taken together, these data do not support a pan-neurogenic function for  SOXB2  genes in the dorsal midbrain, but instead they influence, sequentially, the specification of GABAergic neurons.

Sequential Role of SOXB2 Factors in GABAergic Neuron Specification of the Dorsal Midbrain