During mouse development, the Hedgehog
signalling pathway regulates proliferation in neural progenitors and skin basal
cells. Normally, in the absence of Hedgehog ligand, Patched (PTCH) inhibits
Smoothened (SMO).

In a mouse model, researchers introduce
the SmoM2 constitutively active mutation, which bypasses PTCH inhibition.
Analysis shows persistent Gli transcription factor activity in neural and
epidermal tissues.

Which outcome is most consistent with
constitutive SMO activation in these tissues?

Question

During mouse development, the Hedgehog
signalling pathway regulates proliferation in neural progenitors and skin basal
cells. Normally, in the absence of Hedgehog ligand, Patched (PTCH) inhibits
Smoothened (SMO).

In a mouse model, researchers introduce
the SmoM2 constitutively active mutation, which bypasses PTCH inhibition.
Analysis shows persistent Gli transcription factor activity in neural and
epidermal tissues.

Which outcome is most consistent with
constitutive SMO activation in these tissues?

Answer

Persistent
Gli activation drives uncontrolled proliferation in neural progenitors and
basal epidermal cells

Answer

Gli target genes are
only transiently activated due to partial negative feedback by GLI3 repressor,
limiting tissue overgrowth

Answer

Constitutive SMO
activation leads to developmental arrest due to accumulation of non-functional
Gli proteins

Answer

PTCH upregulation
compensates for SMO activation, preventing tumour formation

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During mouse development, the Hedgehog signalling pathway regulates proliferati...

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