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Cells migrating in response to external stimuli form lamellipodia, which are thin membrane protrusions supported by a mesh of linked, branched, or unbranched actin filaments. These actin filaments interact with myosin motor proteins, creating the dynamic actomyosin complex within the cytoskeleton. Contractility, or the ability to generate contractile stress, is inherent to the actomyosin complex. It helps cells detect the stiffness of the surrounding ECM and exert contractile force for...
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MARCKS and PI(4,5)P2 reciprocally regulate actin-based dendritic spine morphology.

Barbara Calabrese1, Shelley Halpain1

  • 1Department of Neurobiology, School of Biological Sciences, University of California San Diego and Sanford Consortium for Regenerative Medicine, La Jolla, CA 92037.

Molecular Biology of the Cell
|December 13, 2023
PubMed
Summary

Myristoylated, alanine-rich C-kinase substrate (MARCKS) regulates neuronal dendritic spine morphology by controlling phosphatidylinositol-4,5-biphosphate (PI(4,5)P2) levels. Its interaction with PI(4,5)P2 influences actin dynamics and spine shape.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Myristoylated, alanine-rich C-kinase substrate (MARCKS) is a key protein regulating cellular functions.
  • MARCKS binds F-actin and phospholipids, influencing neuronal dendritic spine morphology.
  • The precise mechanism by which MARCKS affects spine morphology, particularly its interaction with PI(4,5)P2, remains unclear.

Purpose of the Study:

  • To investigate the role of MARCKS in regulating dendritic spine morphology through modulation of plasma membrane phosphatidylinositol-4,5-biphosphate (PI(4,5)P2) availability.
  • To test the hypothesis that MARCKS's effects on spine morphology are mediated by its control over PI(4,5)P2 levels.

Main Methods:

  • Manipulating MARCKS concentration and membrane targeting in neurons.
  • Measuring free PI(4,5)P2 levels on the dendritic plasma membrane.
  • Overexpressing phosphatidylinositol-4-phosphate 5-kinase (PIP5K) and inositol polyphosphate 5-phosphatase (5ptase) to alter endogenous PI(4,5)P2 levels.
  • Analyzing changes in dendritic spine morphology and actin properties, including the role of cofilin.

Main Results:

  • Free PI(4,5)P2 concentration on the dendritic plasma membrane was inversely proportional to MARCKS concentration.
  • Overexpression of PIP5K led to spine shrinkage, similar to MARCKS depletion.
  • Overexpression of 5ptase induced spine elongation, mimicking constitutively membrane-bound MARCKS.
  • Observed phenotypes involved alterations in actin properties mediated by cofilin.

Conclusions:

  • MARCKS regulates dendritic spine morphology by controlling the availability of PI(4,5)P2.
  • Neuronal activity likely modulates actin-dependent spine morphology via antagonistic interactions between MARCKS and PI(4,5)P2.