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#competence

3 public questions tagged with this topic.

The ability of a cell to respond to an inducing signal is called:

Competence is defined as time-limited physiological capacity of a tissue to perceive and correctly translate a specific inductive cue into altered fate. Molecular basis includes presence of appropriate receptors, intracellular signal transducers, transcription factor availability and accessible chromatin at target gene loci during critical window. Xenopus ectoderm competence to respond to neural inducers exists only during gastrula stages when FGF receptors and Smad machinery are expressed. After this period, BMP signaling consolidation and chromatin closure extinguish responsiveness. Loss of competence involves receptor downregulation, upregulation of inhibitors and epigenetic silencing, ensuring inductive events occur sequentially and preventing ectopic induction later.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 4: Competence Windows in Embryonic Induction.

Which of the following correctly defines competence in cell specification?

Competence describes transient window during which a cell or tissue possesses ability to receive and correctly interpret a specific inductive signal. Molecular basis includes expression of appropriate receptors, intracellular transducers and accessible chromatin at target gene loci. For example, Xenopus animal cap ectoderm is competent to respond to mesoderm inducers like Activin only between mid-blastula and early gastrula, when FGF receptors and Smad machinery are present. After this period, BMP dominance and chromatin closure extinguish responsiveness. Loss of competence involves receptor downregulation, inhibitor induction and epigenetic silencing, temporally restricting inductive interactions and ordering developmental events.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 4: Competence and Inductive Responsiveness.

Which transcription factor is essential for making head ectoderm competent to respond to optic vesicle signals?

Head ectoderm acquires ability to form lens long before optic vesicle contact, a property called competence. Pax6, a paired-homeodomain transcription factor, marks the entire preplacodal region and maintains chromatin accessible for lens-specific enhancers like FoxE3 and Sox2. Without Pax6, surface ectoderm fails to upregulate crystallins even when grafted with a wild-type optic vesicle. Fujiwara rat recombination experiments showed mutant ectoderm non-responsive, proving Pax6 functions intrinsically in ectoderm competence rather than inductive signal production, enabling subsequent BMP and FGF mediated differentiation.

Ref: Gilbert, Developmental Biology, 12th ed., Chapter 7: Lens competence and Pax6 requirement in surface ectoderm.