Fig. 4.

Gadd45γ mediates β-catenin–dependent fate response in NSCs. (A) The role of Gadd45γ in NSC neurogenesis and apoptosis was determined by probing cell fate within naive NSCs, NSCs engineered for KD of endogenous Gadd45γ, or in either cell line engineered to express exogenous Gadd45γ. Cells were subjected to either sustained or transient β-catenin signaling (3 μm CHIR) and were fixed at 72 h. (B) Loss of neurogenesis under Gadd45γ KD is restored by ectopic Gadd45γ expression. (C) Gadd45γ KD prevents apoptosis that is normally induced by transient β-catenin activation, but apoptosis is only marginally restored with ectopic Gadd45γ expression. (D) Ectopic Gadd45γ expression reduces apoptosis and increases neurogenesis in wild-type (wt) NSCs in response to transient β-catenin stimulation. White circles represent the means of individual experiments. Gray circles represent the means of biological replicates within experiments (each replicate mean obtained from 300 to 3,000 cells). Dashed lines indicate baseline values (no β-catenin stimulus).