More from the tortured world of gene-centricity.
Further to: How much does DNA influence cell shape (“In short, we don’t know how even these single cells get their shape, and it doesn’t seem to be as simple as “from their DNA, moron!”):
Come all you budding Darwinians, and you will hear the truth about how DNA rules, the selfish gene is the most important concept in science ever, and Darwin’s is the single greatest idea anyone ever had.
For our demonstration, we will use the humble tooth. A friend writes to mention a mouse experiment where developing tooth buds were moved so that the incisors and the molars were switched. The tooth buds became the tooth appropriate to the switched location, not the original one, in direct contrast to what we would expect from a gene’centric view. Apparently, developing tooth cells alter their transcription and development in response to signals from the gum tissue. He thinks this is also why human bicuspids (premolars) look weird. They are getting signals from both tissue locations.
Here is the conclusion from one article:
This study provides the first comprehensive analysis of differential gene expression between developing murine tooth types, leading to new insights into the regulatory mechanisms involved in the ontogenesis of mammalian teeth. Molecules belonging to pathways involved in various aspects of development (such as the Wnt, TGFß/BMP, or FGF pathways) were discovered as potentially carrying information for differential tooth morphogenesis. Of interest is the involvement of the retinoic acid pathway [76], as retinoids have marked effects on molar and incisor morphogenesis [22,77]. Tooth morphology and its evolution in various mammalian species were proven to be related to dosage effect of signaling molecules, like for instance FGF3 being able to modify the cusps pattern [16,78]. Our microarray analysis highlighted molecules more or less strongly expressed in a given tooth type, reinforcing the model of dosage modulating mechanisms. Gene dosage abnormalities are likely to occur in human rare diseases presenting with a tooth family specific dental phenotype [37,38,79]. Some of the corresponding genes were not retrieved in our analysis of differential gene expression in lower incisors versus lower or upper molars, suggesting that other levels of regulation, post-transcriptionally via effectors of a given pathway or via fine tuning of kinase signaling (e.g. ref. [80]), will undoubtedly also participate in the molecular identity leading to specific tooth morphology. Future investigation of differential gene expressions between upper and lower incisors, two similar tooth types formed from neural crest cells of different origins, might also contribute to shed light on specific morphogenesis and its link to individual tooth shape.
See also: Here and here. Thank to David A. DeWitt for citations.
See also: “If DNA really rules, why did THIS happen?”, where human neurons, transplanted into a mouse, had a mouse morphology.
Jonathan Wells: Far from being all-powerful, DNA does not wholly determine biological form (Mutate a fruit fly embryo in every possible way, and observe only three possible outcomes: a normal fruit fly, a defective fruit fly, or a dead fruit fly.)
Jonathan Wells: We are far from a good theoretical model of organisms’ development (We are far from having a complete list of the components, as a matter of fact.)
Note: Mice don’t usually have bicuspids (premolars) between the incisors and molars but they may appear in mice as supernumerary (extra) teeth.
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