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FatJ acts via the Hippo mediator Yap1 to restrict the size of neural progenitor cell pools

Nick J Van Hateren1, Raman M Das, Guillaume M Hautbergue

  • 1MRC Centre for Developmental and Biomedical Genetics, University of Sheffield, Sheffield, S10 2TN, UK.

Development (Cambridge, England)
|April 28, 2011
PubMed

Insights

FatJ cadherin regulates neural progenitor cell numbers in the developing spinal cord. Loss of FatJ increases progenitor and neuron numbers by impacting the Hippo-Yap1 pathway.

Area of Science:

  • Developmental biology
  • Neuroscience
  • Cell biology

Background:

  • Spinal cord development relies on precise control of progenitor and differentiated cell numbers.
  • Mechanisms regulating cell numbers along the neural tube's dorsoventral axis are poorly understood.

Purpose of the Study:

  • To investigate the role of FatJ cadherin in controlling neural progenitor cell numbers.
  • To elucidate the molecular pathways involved in FatJ-mediated cell number regulation.

Main Methods:

  • Conducted a large-scale RNA interference (RNAi) screen in the chick embryonic neural tube.
  • Utilized FatJ loss-of-function models to assess effects on progenitor and neuron populations.
  • Investigated interactions with the Hippo pathway components, including Yap1.

Main Results:

  • FatJ cadherin is localized to neural progenitors in intermediate regions of the neural tube.
  • Loss of FatJ function leads to an increase in dp4-vp1 progenitors and Lim1(+)/Lim2(+) neurons.
  • FatJ's regulatory function is mediated through the Hippo pathway, specifically involving Yap1.

Conclusions:

  • RNAi screening is a viable method for studying the chick embryonic neural tube.
  • FatJ acts via the Hippo-Yap1 pathway to regulate cell proliferation and differentiation in specific neural progenitor pools.
  • This study identifies a novel mechanism controlling cell numbers crucial for spinal cord development.

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