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Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
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Ppargc1a Controls Ciliated Cell Development by Regulating Prostaglandin Biosynthesis.

Joseph M Chambers1, Amanda Addiego1, Ana L Flores-Mireles2

  • 1Department of Biological Sciences, Center for Stem Cells and Regenerative Medicine, Center for Zebrafish Research, Boler-Parseghian Center for Rare and Neglected Diseases, University of Notre Dame, Notre Dame, IN 46556, USA.

Cell Reports
|November 11, 2020
PubMed
Summary
This summary is machine-generated.

Peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (ppargc1a) is crucial for cilia formation and kidney cell development. Restoring prostaglandin signaling with PGE2 or ptgs1 can rescue these defects in ppargc1a-deficient models.

Keywords:
PGC1αPpargc1aciliogenesisdevelopmentkidneymulticiliated cellnephronprostaglandinzebrafish

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Cilia are vital microtubule-based organelles involved in sensing and fluid movement.
  • Dysfunctional cilia lead to ciliopathies, a class of human diseases.
  • Ciliogenesis, the process of cilia formation, requires precise genetic regulation.

Purpose of the Study:

  • To investigate the role of peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (ppargc1a) in ciliogenesis and ciliated cell fate.
  • To elucidate the molecular mechanisms by which ppargc1a regulates these processes.

Main Methods:

  • Analysis of ppargc1a function in nodal, mono-, and multiciliated cells (MCCs) during embryogenesis.
  • Investigating the impact of ppargc1a deficiency on prostaglandin signaling pathways.
  • Utilizing prostaglandin E2 (PGE2) treatment and ptgs1 gene manipulation (overexpression and knockdown) in ppargc1a-deficient models.

Main Results:

  • ppargc1a is essential for ciliogenesis across various cell types and for renal tubule ciliated cell differentiation.
  • ppargc1a regulates ciliogenesis and cell fate through prostaglandin signaling.
  • Genetic disruption of ppargc1a specifically decreases prostaglandin-endoperoxide synthase 1 (ptgs1) expression.
  • PGE2 treatment or ptgs1 overexpression rescues ciliogenesis and renal MCC development in ppargc1a-deficient embryos.

Conclusions:

  • ppargc1a acts as a critical regulator of prostaglandin signaling during the development of ciliated cells.
  • Dysregulation of ppargc1a impacts cilia formation and cell fate determination.
  • Targeting the ppargc1a-prostaglandin pathway offers potential therapeutic avenues for ciliopathies.