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BTG4 is a meiotic cell cycle-coupled maternal-zygotic-transition licensing factor in oocytes

Chao Yu1, Shu-Yan Ji1, Qian-Qian Sha1

  • 1Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.

Nature Structural & Molecular Biology
|April 12, 2016
PubMed

Insights

B-cell translocation gene-4 (BTG4) is crucial for maternal mRNA decay during the maternal-zygotic transition (MZT) in mice. Its absence causes infertility due to developmental arrest, highlighting its role in oocyte maturation and embryonic development.

Area of Science:

  • Reproductive Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • Maternal mRNA decay is essential during the maternal-zygotic transition (MZT) but the underlying mechanisms remain unclear.
  • Oocyte meiotic progression is linked to maternal mRNA stability, yet factors initiating decay are unknown.

Purpose of the Study:

  • To identify factors regulating maternal mRNA decay during oocyte maturation.
  • To elucidate the role of B-cell translocation gene-4 (BTG4) in the maternal-zygotic transition (MZT) and oocyte development.

Main Methods:

  • Identification of BTG4 as an MZT licensing factor in mice.
  • Investigating the interaction between BTG4, CNOT7 (CCR4-NOT deadenylase), and eIF4E (translation initiation factor).
  • Analyzing Btg4-null mouse models for fertility and developmental outcomes.

Main Results:

  • BTG4 facilitates maternal mRNA decay by bridging CNOT7 and eIF4E.
  • Btg4-null female mice exhibit infertility with early developmental arrest, despite producing normal oocytes.
  • MAP kinase cascade triggers Btg4 mRNA translation, linking mRNA decay to oocyte maturation and fertilization.

Conclusions:

  • BTG4 is a key regulator of maternal mRNA decay, essential for oocyte cytoplasmic maturation.
  • The BTG4-mediated pathway couples mRNA decay with meiotic maturation, determining mammalian embryo developmental potential.

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