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Hox Genes Regulate Digit Patterning by Controlling the Wavelength of a Turing-Type Mechanism

Digit Determination Pentadactyly has been an early and rapid innovation of tetrapods. Sheth et al. (p. 1476) report that a dramatic reduction in distally expressed Hox genes, in the absence of a functional morphogen signaling pathway, results in extreme polydactyly in mice. Mutant digits exhibited patterns reminiscent of the endoskeleton of fins, suggesting that an ancestral patterning mechanism has been deeply conserved in evolution. Mouse genetics and computer modeling suggest that a reaction-diffusion mechanism defines digit pattern. The formation of repetitive structures (such as stripes) in nature is often consistent with a reaction-diffusion mechanism, or Turing model, of self-organizing systems. We used mouse genetics to analyze how digit patterning (an iterative digit/nondigit pattern) is generated. We showed that the progressive reduction in Hoxa13 and Hoxd11-Hoxd13 genes (hereafter referred to as distal Hox genes) from the Gli3-null background results in progressively more severe polydactyly, displaying thinner and densely packed digits. Combined with computer modeling, our results argue for a Turing-type mechanism underlying digit patterning, in which the dose of distal Hox genes modulates the digit period or wavelength. The phenotypic similarity with fish-fin endoskeleton patterns suggests that the pentadactyl state has been achieved through modification of an ancestral Turing-type mechanism.