21-P027 Clonal deletion of RET using mosaic analysis with double markers (MADM) in the enteric nervous system

functions. However, the mechanisms of GABAergic neurogenesis in the midbrain are not well understood. Previously, it has been shown that Ascl1 is required for development of GABAergic neurons in the midbrain. Here we have characterized in more detail the role of Ascl1 in the development of distinct subpopulations of midbrain GABAergic neurons. In Ascl1-null mutants GABAergic neurons are completely absent in the dorsal part of the midbrain. Ventrally part of the cells differentiate but the amount of GABAergic neurons is reduced.Tracing back to the origin of these defects we show that Ascl1 is regulating differently both GABAergic neurogenesis and neuronal subtype specification in distinct subpopulations of the ventral midbrain. We are currently conducting additional studies to further specify the ventral GABAergic populations that are affected in the Ascl1 mutants and to examine the downstream differentiation factors involved in the GABAergic neurogenesis.Results towards understanding the molecular and developmental mechanisms regulated by Ascl1 will be presented.