You are currently viewing the summary.
View Full TextLog in to view the full text
AAAS login provides access to Science for AAAS members, and access to other journals in the Science family to users who have purchased individual subscriptions.
More options
Download and print this article for your personal scholarly, research, and educational use.
Buy a single issue of Science for just $15 USD.
Summary
Alan Turing is best known as the father of theoretical computer sciences and for his role in cracking the Enigma encryption codes during World War II. He was also interested in mathematical biology and published (1) a theoretical rationale for the self-regulation and patterning of tissues in embryos. The so-called reaction-diffusion model allows mathematical simulation of diverse types of embryonic patterns with astonishing accuracy (1–3). During the past two decades, the existence of Turing-type mechanisms has been experimentally explored and is now well established in developmental systems such as skin pigmentation patterning in fishes, and hair and feather follicle patterning in mouse and chicken embryos (3). However, the extent to which Turing-type mechanisms control patterning of vertebrate organs is less clear. Often, the relevant signaling interactions are not fully understood and/or Turing-like features have not been thoroughly verified by experimentation and/or genetic analysis (3). Raspopovic et al., on page 566 in this issue, now make a good case for Turing-like features in the periodic pattern of digits by identifying the molecular architecture of what appears to be a Turing network functioning in positioning the digit primordia within mouse limb buds (4).
