The neural plate forms because the organizer (notochord) secretes neural-inducing signals that directly activate neural genes in the overlying ectoderm.
TTrue
FFalse
Answer: False
The 'default model' of neural induction, supported by substantial evidence, proposes that ectoderm's default fate IS neural — not epidermal. BMP signaling actively suppresses neural fate and promotes epidermis. The organizer does not secrete neural activators; instead, it secretes BMP antagonists (Chordin, Noggin, Follistatin) that block BMP signaling in the overlying ectoderm, allowing it to adopt its default neural fate. Neural induction is thus an act of inhibition removal (de-repression), not direct activation. This was demonstrated when dissociated ectodermal cells, freed from BMP signaling by their neighbors, spontaneously adopted neural fate without any inducer.
Question 2 Multiple Choice
Neural crest cells originate at the boundary between the neural plate and non-neural ectoderm. Which of the following is NOT a derivative of neural crest cells?
APeripheral sensory neurons and glia
BMelanocytes (pigment cells)
CCraniofacial bone and cartilage
DSkeletal muscle of the limbs
Neural crest cells are remarkably multipotent, contributing to an astonishing variety of cell types: peripheral neurons and glia, melanocytes, craniofacial bone and cartilage (an unusual exception to the rule that bone derives from mesoderm), smooth muscle of great vessels, adrenal medulla chromaffin cells, and more. Skeletal muscle, however, derives from somitic mesoderm (specifically the myotome), not from neural crest. The neural crest is sometimes called the 'fourth germ layer' because of its diverse contributions, which span derivatives traditionally associated with all three classical germ layers.
Question 3 Short Answer
Explain why folic acid supplementation reduces the incidence of neural tube defects.
Think about your answer, then reveal below.
Model answer: Folic acid is essential for nucleotide synthesis (providing one-carbon units for purine and thymidylate biosynthesis) and for methylation reactions. Neural tube closure requires rapid cell proliferation (to generate enough cells for the neural folds to meet and fuse) and precisely regulated gene expression (dependent on DNA and histone methylation). Folate deficiency impairs both processes: insufficient nucleotides slow cell division, and inadequate methylation disrupts gene regulation needed for neural fold elevation and fusion. Supplementation ensures adequate folate for these critical processes during the narrow developmental window of neural tube closure (days 21-28 in humans), reducing but not eliminating neural tube defects because genetic susceptibility and other environmental factors also contribute.
Public health recommendations for folic acid supplementation before and during early pregnancy have reduced neural tube defect incidence by approximately 50-70%. This is one of the most successful applications of developmental biology knowledge to preventive medicine.