{"id":10,"title":"Maternal β-catenin regulates trophectoderm development in mouse preimplantation embryos","title_zh":"母源β-catenin调控小鼠植入前胚胎滋养外胚层发育","url":"https://pubmed.ncbi.nlm.nih.gov/42983064","doi":"10.1007/s11427-026-3470-5","pmid":"42983064","journal":"Sci China Life Sci","kind":"paper","lang":"en","published_at":"2026-10-30T00:00:00+00:00","fetched_at":"2026-11-08T03:43:49+00:00","authors":["Tian L","Jin H","Han Y","Zheng T","Zhang T","Liu B","Huang H","Xing C","Wu X","Meng A"],"primary_topic":"early-embryo","topics":[{"slug":"early-embryo","score":8.0,"hits":["blastocyst","compaction","gastrulation","preimplantation embryo","trophectoderm"]},{"slug":"embryology-lab","score":1.0,"hits":["embryo quality"]},{"slug":"omics-methods","score":1.0,"hits":["transcriptome"]},{"slug":"animal-models","score":0.8,"hits":["mouse embryos"]}],"topic_score":8.0,"preference_score":12.0,"preference_labels":["早期胚胎转录组/单细胞转录组"],"llm_score":78.0,"final_score":96.0,"score_dims":{"novelty":82,"rigor":80,"impact":72,"relevance":85,"translation":62},"recommend_reason":"挑战“母源CTNNB1对囊胚发育可有可无”的既有认识，用遗传学、转录组与挽救实验串起Wnt–ERK–CCND1轴与TE增殖，对理解囊胚质量与培养干预（如bFGF）有直接启发。","keywords":["母源β-catenin/CTNNB1","滋养外胚层","囊胚形成","MAPK/ERK","母源效应基因","植入前胚胎"],"selected":1,"story_id":279,"llm_provider":"deepseek","llm_model":"deepseek-flash","llm_effort":"low","source_key":"pubmed-embryo-omics","source_name":"PubMed · 胚胎/卵母细胞组学","source_tier":1,"mention_count":2,"has_interpretation":false,"journal_key":"sci-china-ls","journal_tier":"general-top","journal_if":8.0,"is_mock":false,"summary_zh":"该研究在小鼠中重新审视母源β-catenin（CTNNB1）在植入前发育中的作用：既往认为其可缺失，作者却发现母源CTNNB1在受精后激活经典Wnt信号、维持囊胚形成所必需。母源Ctnnb1缺失导致发育延迟、致密化受损、滋养外胚层（TE）细胞数减少及E18.5发育缺陷；转录组显示细胞周期、MAPK/ERK与凋亡通路广泛失调。bFGF处理或过表达Ctnnb1、Erk2、Ccnd1可部分挽救表型。机制上，母源CTNNB1促进pERK1/2核积聚与Ccnd1转录，维持TE增殖。","summary":"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.","interpretation_basis":null,"fulltext_status":"not_found","interpretation":null,"fulltext":{"available":false,"status":"not_found","reason":"Europe PMC 无此记录：DOI 10.1007/s11427-026-3470-5","pmcid":null,"license":null,"chars":0,"source":"Europe PMC","fetched_at":"2026-11-08T03:59:09+00:00"}}