β-Catenin/CTNNB1 is the key intracellular effector of the canonical Wnt signaling. While zygotic CTNNB1 is essential for gastrulation in mouse embryos, maternal CTNNB1 is thought to be dispensable for development to the blastocyst stage. Besides, it remains controversial whether maternal CTNNB1 is activated during preimplantation stages. In this study, we report that maternal CTNNB1 is required for activating canonical Wnt signaling after fertilization and sustaining robust blastocyst formation. Loss of maternal CTNNB1 causes developmental delay, impaired compaction, reduced trophectoderm (TE) cell number, and developmental defects at E18.5. Transcriptome profiling highlights widespread dysregulation of cell-cycle, MAPK/ERK, and apoptosis pathways. Treatment with basic fibroblast growth factor (bFGF) or overexpression of Ctnnb1, Erk2, or Ccnd1 can partially rescue preimplantation defects in maternal Ctnnb1 (MCtnnb1) mutant embryos. Mechanistically, maternal CTNNB1 promotes nuclear accumulation of phosphorylated ERK1/2 (pERK1/2) and transcription of Ccnd1 to sustain TE proliferation and robust blastocyst formation. Taken together, our findings shed light on the role of maternal CTNNB1 signaling in supporting preimplantation embryo quality in mammals.