A transiently expressed connexin is essential for anterior neural plate development in Ciona intestinalis

Christopher Hackley1, Erin Mulholland, Gil Jung Kim

  • 1Department of Molecular, Cellular and Developmental Biology, University of California Santa Barbara, Santa Barbara, CA 93106, USA.

Development (Cambridge, England)
|November 24, 2012
PubMed

Insights

The frimousse mutation disrupts neural plate development in Ciona intestinalis by affecting connexin (cx-11) gene function. This highlights the critical role of intercellular communication via gap junctions in neural induction.

Area of Science:

  • Developmental Biology
  • Neuroscience
  • Genetics

Background:

  • The development of the anterior neural plate is crucial for establishing the central nervous system.
  • Intercellular communication mechanisms underlying neural induction are not fully understood.

Purpose of the Study:

  • To identify genetic factors regulating anterior neural plate development in Ciona intestinalis.
  • To elucidate the role of connexin-mediated signaling in neural induction.

Main Methods:

  • Forward genetic screen in Ciona intestinalis to identify mutants with neural development defects.
  • Molecular cloning to identify the genetic lesion in the 'frimousse' mutant.
  • Live imaging using a genetically encoded calcium indicator to monitor calcium transients.
  • Pharmacological inhibition of gap junctions and calcium signaling.

Main Results:

  • The 'frimousse' mutation disrupts anterior neural plate development, causing cells to default to an epidermal fate.
  • The mutation lies in the connexin gene cx-11, expressed during neural induction.
  • Wild-type embryos exhibit calcium transients in the neural plate, which are absent in 'frimousse' mutants.
  • Inhibition of calcium transients or gap junctions phenocopies the 'frimousse' mutation.

Conclusions:

  • Connexin-11 (cx-11) is essential for maintaining anterior neural plate fate in Ciona intestinalis.
  • Intercellular communication through gap junctions, likely mediated by calcium transients, is crucial for Ciona intestinalis neural induction.

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