Neural Development and Crest Migration

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Questions and Answers

Which adhesion protein is primarily expressed in the surface ectoderm?

  • Cadherin-6B
  • N-cadherin
  • E-cadherin (correct)
  • RhoA

What role does Snail-2 play in the premigratory neural crest domain?

  • It activates cadherin-6B.
  • It enhances apoptosis in neural crest cells.
  • It represses N-cadherin and E-cadherin. (correct)
  • It promotes N-cadherin expression.

What initiates delamination in the apical half of premigratory neural crest cells?

  • High levels of BMP
  • Activation of N-cadherin
  • Cadherin-6B activity (correct)
  • Upregulation of E-cadherin

Which signaling pathway establishes the polar activity of RhoA and Rac1 during neural crest cell migration?

<p>Noncanonical Wnt signaling (C)</p> Signup and view all the answers

What occurs during contact inhibition of locomotion between neural crest cells?

<p>Cytoskeletal changes halt protrusive activity. (A)</p> Signup and view all the answers

Flashcards

Differentiation of neuroepithelium regions

BMP and Wnt signaling pathways determine the three main areas of the neuroepithelium: the surface ectoderm, neural tube, and premigratory neural crest. These regions are identified by their unique adhesion proteins: E-cadherin (surface ectoderm), N-cadherin (neural tube), and cadherin-6B (premigratory neural crest).

Premigratory neural crest cell specification

The premigratory neural crest cells exhibit high BMP levels and moderate Wnt levels, leading to the expression of Snail-2 protein. Snail-2 represses the expression of N-cadherin and E-cadherin, allowing these cells to detach from their original location.

Neural crest delamination

Cadherin-6B, present on the apical half of premigratory neural crest cells, activates RhoA and actomyosin contractile fibers, causing apical constriction and initiating delamination. This process allows the neural crest cells to detach from the neural tube and start their migration.

Noncanonical Wnt signaling - Guiding neural crest migration

Noncanonical Wnt signaling controls the directionality of migrating neural crest cells by regulating the activity of RhoA and Rac1 proteins. RhoA (red) and Rac1 (yellow) are responsible for extending and retracting cellular protrusions, guiding the cells along their migratory path.

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Contact inhibition of neural crest migration

When neural crest cells encounter each other, they exhibit contact inhibition of locomotion, causing them to halt their migration, change direction, and disperse. This behavior occurs because contact depolymerizes the cytoskeleton of the cells, inhibiting protrusive activity along the contact point and promoting new protrusions away from the point of contact.

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Study Notes

Neural Tube and Epidermis Formation

  • Neural and surface ectoderms separate and fuse at the midline to form the neural tube and epidermis, respectively.

Regional Specification of Neuroepithelium

  • BMP and Wnt signals define three neuroepithelial regions:
    • Surface ectoderm (E-cadherin)
    • Neural tube (N-cadherin)
    • Premigratory neural crest (cadherin-6B)

Premigratory Neural Crest Characteristics

  • BMP levels are highest, Wnt levels are intermediate in the premigratory domain.
  • This promotes Snail-2 expression.
  • Snail-2 represses N-cadherin and E-cadherin.
  • Cadherin-6B is expressed in the premigratory neural crest apical half.
  • Cadherin-6B activates RhoA and actomyosin, leading to constriction and delamination.

Neural Crest Cell Migration

  • Noncanonical Wnt signaling establishes RhoA and Rac1 polarity along the migratory axis.
  • Contact inhibition of locomotion occurs when cells touch.
  • Contacting cells stop, turn, and migrate in the opposite direction.
  • Depolymerizing activity in the cytoskeleton prevents protrusion at contacting surfaces, with new protrusive extensions forming elsewhere.
  • This dispersal behavior occurs wherever cells are in close contact, excluding leading edge protrusions.

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