Practice question

Polydactyly reflecting supernumerary digits often arises from dysregulation of SHH-Gli3 and distal Hox networks controlling digit periodicity. Mutations in HOXD13, particularly polyalanine tract expansions, cause synpolydactyly with fused extra digits due to altered transcriptional regulation of autopod patterning and ectopic activation of anterior Gli3 processing leading to broadened SHH targets. Tbx4 dictates hindlimb identity, Pax6 eye development, FGF10 limb initiation. HOXD13 normally limits digit number controlling interdigital proliferation and termination timing, thus mutation disrupts fine-tuning leading to polydactylous phenotype in mammals.