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PIP5K1A-PIP2-RhoA Signaling Orchestrates Membrane Remodeling during Early Porcine Embryo Development.

Cheng-Lin Zhan1, Song-Hee Lee1, Zheng-Wen Nie1,2

  • 1Department of Animal Science, Chungbuk National University, Cheongju 28644, Republic of Korea.

International Journal of Biological Sciences
|May 29, 2026
PubMed
Summary

Phosphatidylinositol-4-phosphate 5-kinase type I alpha (PIP5K1A) regulates mammalian embryo development by controlling membrane remodeling and actin dynamics. Its proper function is crucial for oocyte activation and early embryonic cell division.

Keywords:
PIP5K1Acalcium oscillationcytoskeletal dynamicsmembrane remodelingphosphoinositide signaling

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Biochemistry

Background:

  • Dynamic plasma membrane remodeling is essential for mammalian embryogenesis, including cleavage and signal transduction.
  • Oocyte activation involves membrane remodeling and increased phosphatidylinositol (4,5)-bisphosphate (PIP2) levels, but regulatory mechanisms are unclear.

Purpose of the Study:

  • To identify key regulators of membrane remodeling during mammalian oocyte activation and early embryonic development.
  • To elucidate the role of phosphatidylinositol-4-phosphate 5-kinase type I alpha (PIP5K1A) in regulating membrane dynamics and cytoskeletal organization.

Main Methods:

  • Investigated the function of PIP5K1A in porcine embryos using maternal depletion and overexpression techniques.
  • Performed structure-function analysis of PIP5K1A, including residue mutation and domain analysis.
  • Examined interactions with RhoA and downstream signaling pathways like phospholipase C-inositol trisphosphate-Ca2+.

Main Results:

  • Maternal depletion of PIP5K1A disrupted oocyte activation, actin organization, vesicle trafficking, and blocked early development.
  • Excessive PIP5K1A expression led to PIP2 vesicle accumulation, actin trapping, reduced membrane contractility, and cleavage failure.
  • PIP5K1A interacts with RhoA, localizes to the plasma membrane via its PIPB motif, and its catalytic activity is essential for RhoA localization and endocytic processes.

Conclusions:

  • PIP5K1A is a critical regulator of membrane remodeling, essential for oocyte activation and early mammalian embryonic development.
  • PIP5K1A coordinates lipid signaling, actin dynamics, and membrane contractility through interactions with RhoA and sustained Ca2+ signaling.
  • Dysregulation of PIP5K1A impacts embryonic development, highlighting its role as a central organizer of cellular processes during embryogenesis.