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Anillin localization defect in cardiomyocyte binucleation.

Felix B Engel1, Michael Schebesta, Mark T Keating

  • 1Department of Pediatrics, Harvard Medical School, and Department of Cardiology, Children's Hospital, 320 Longwood Avenue, Boston, MA 02115, USA. engel@enders.tch.harvard.edu

Journal of Molecular and Cellular Cardiology
|August 8, 2006
PubMed
Summary
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Postnatal cardiomyocytes can divide their DNA but not their cells, leading to binucleation. This study reveals that defects in Anillin protein localization and p38 activity cause this cytokinesis failure.

Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Developmental Biology

Background:

  • Heart growth in early development relies on cardiomyocyte proliferation.
  • Postnatal heart growth occurs via cardiomyocyte cell enlargement, not proliferation.
  • Postnatal cardiomyocytes can enter mitosis but fail to complete cytokinesis, resulting in binucleation.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying cytokinesis failure in postnatal cardiomyocytes.
  • To determine if contractile element disassembly or other factors inhibit cytokinesis.
  • To identify key proteins and pathways involved in cardiomyocyte binucleation.

Main Methods:

  • Analysis of cardiomyocyte cell division, including DNA synthesis, mitosis, and cytokinesis.

Related Experiment Videos

  • Immunofluorescence microscopy to assess the localization of key cell division proteins like Aurora B and Anillin.
  • Pharmacological inhibition of p38 kinase to evaluate its role in cytokinesis.
  • Microarray analysis to identify gene expression changes following p38 inhibition.

    • Main Results:

    • Serum-induced binucleation involves normal contractile apparatus disassembly.
    • Binucleation is characterized by asymmetric furrow constriction, delayed furrowing, and defective mid-body formation.
    • Anillin protein shows abnormal localization during cytokinesis, failing to focus at the cortex and exhibiting expanded mid-body localization.
    • p38 kinase accumulates at the mid-body during cytokinesis, and its inhibition rescues mid-body formation defects.
    • p38 inhibition leads to the upregulation of central spindle components.

    Conclusions:

    • Postnatal cardiomyocytes initiate cleavage furrow formation but exhibit cytokinesis defects leading to binucleation.
    • Abnormal Anillin localization is a key feature of cardiomyocyte binucleation.
    • p38 kinase activity plays a crucial regulatory role in cardiomyocyte cytokinesis and mid-body organization.