Bei Wang, Jason E. Long, Pierre Flandin, Ramon Pla, Ronald R. Waclaw, Kenneth Campbell and John L.R. Rubenstein Loss of Gsx1 and Gsx2 function rescues distinct phenotypes in Dlx1/2 mutants Journal of Comparative Neurology 521
Dlx1/2 mutant mice have deficits in subpallial differentiation, including overexpression of Gsx1 and Gsx2. To investigate whether Gsx overexpression contributes to the Dlx1/2−/− phenotypes, we made compound loss-of-function mutants. Gsx2;Dlx1/2 mutants showed partial rescue of the increased expression of Notch-signaling mediators. On the other hand, Gsx1;Dlx1/2 mutants resulted in a partial rescue of interneuron migration to the cortex. Thus, despite their redundant properties, Gsx1 and Gsx2 have distinct interactions with Dlx1 and 2.
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