In “On the difficulty of increasing dental complexity” (Nature, 07 March 2012),
Enni Harjunmaa and colleagues report,
One of the fascinating aspects of the history of life is the apparent increase in morphological complexity through time, a well known example being mammalian cheek tooth evolution. In contrast, experimental studies of development more readily show a decrease in complexity, again well exemplified by mammalian teeth, in which tooth crown features called cusps are frequently lost in mutant and transgenic mice. Here we report that mouse tooth complexity can be increased substantially by adjusting multiple signalling pathways simultaneously. We cultured teeth in vitro and adjusted ectodysplasin (EDA), activin A and sonic hedgehog (SHH) pathways, all of which are individually required for normal tooth development. We quantified tooth complexity using the number of cusps and a topographic measure of surface complexity. The results show that whereas activation of EDA and activin A signalling, and inhibition of SHH signalling, individually cause subtle to moderate increases in complexity, cusp number is doubled when all three pathways are adjusted in unison. Furthermore, the increase in cusp number does not result from an increase in tooth size, but from an altered primary patterning phase of development. The combination of a lack of complex mutants, the paucity of natural variants with complex phenotypes, and our results of greatly increased dental complexity using multiple pathways, suggests that an increase may be inherently different from a decrease in phenotypic complexity.
These people may be advancing an ID argument, though they do not appear to know it, and no careers should be harmed in the process.
They say that 1) tooth complexity increases over time. 2) complexity is usually lost when closely observed in the laboratory (and no one is doing anything to preserve it). 3) they went to some trouble to preserve tooth complexity and succeeded.
A logical conclusion is that natural selection degrades complexity and that complexity is preserved by design. Thoughts?
Meanwhile, a flustered correspondent writes to say,
Mike Behe could have written this article! Harjunmaa et al.’s argument: known dental mutants (in mammals) invariably show a decrease in complexity, losses of structure, etc. What is never observed, however, are increases in complexity (e.g., novel cusps). Their hypothesis:
“…substantial increase in complexity can also be proposed to require simultaneous changes in several signalling pathways (or multiple changes in a single pathway). This requirement of multiple changes can be conceptualized as ‘economics of signalling’ in which, for example, increasing signalling through one pathway alone may deplete other signals required to produce a greater number of cusps. In genetic terms, this would approximate a polygenic effect.”
In short, an ID argument – coordinating multiple independent mutations is too unlikely, hence, never observed – in all but name.
Are teeth the new eyes, or what?
Like, it used to be we were hearing that Darwin trembled before the eye (for good reason), but his followers cooked up some nonsense which doesn’t really work but you don’t dare say so.
But if teeth are also a problem now … teeth?