Questions: Induction and Competence

Question 1

Spemann showed that the dorsal lip of the blastopore (organizer) can induce a second neural axis when transplanted to the ventral side. If the same transplant is performed at a much later stage (after neural tube closure), no second axis forms. Why?

• A. The organizer loses its ability to secrete signals at later stages
• B. The ventral ectoderm has lost its competence to respond to neural-inducing signals — the temporal window during which ectoderm can be redirected from epidermal to neural fate has closed
• C. The transplanted cells are rejected by the immune system at later stages
• D. Neural induction only works in one specific species of frog

Answer: (B)

Competence is time-limited. During gastrulation, ventral ectoderm expresses the receptors and downstream transcription factors needed to respond to neural-inducing signals (BMP inhibitors from the organizer). After the competence window closes, the ectoderm's chromatin state changes — neural gene promoters become inaccessible, epidermal commitment is locked in, and the same signals no longer elicit a neural response. This temporal restriction of competence ensures that inductive events occur in the correct developmental sequence and prevents aberrant tissue formation at inappropriate stages.

Question 2

Induction is a one-directional process: the inducer signals and the responder responds, with no feedback from responder to inducer.

• T. True
• F. False

Answer: False

Many inductive interactions are reciprocal — the responder signals back to the inducer, modifying its behavior. A classic example is kidney development: the ureteric bud (inducer) signals to the metanephric mesenchyme (responder) to form nephrons, but the mesenchyme simultaneously signals back to the ureteric bud to promote its branching. Without reciprocal signaling, neither tissue develops properly. This reciprocal induction is common in organogenesis and creates interdependent tissue interactions where each tissue requires signals from the other.

Question 3

What molecular changes underlie the loss of competence in a responding tissue?

Model answer: Loss of competence involves changes at multiple levels: downregulation of receptors for the inductive signal (the tissue can no longer detect the signal), changes in intracellular signaling components (even if some signal reaches the cell, it cannot be transduced), and epigenetic changes in chromatin state (target gene promoters become inaccessible through histone modification or DNA methylation, making them unresponsive even if the upstream signaling pathway is activated). The responding tissue essentially closes the molecular doors through which the inductive signal would act, committing irreversibly to its current fate. Competence is thus a property of the entire signal-reception-to-gene-activation chain, not just receptor availability.

This multi-level restriction of competence makes developmental transitions robust — once a tissue passes the competence window, it cannot be redirected by aberrant signals. This is functionally important for preventing teratomas and ensuring orderly sequential development.