Neoteny: also called juvenilization or pedomorphism, is the retention, by adults in a species, of traits previously seen only in juveniles.
Stated as such, neoteny sounds like just a neat biological trick, resulting in interesting specimens. One might go on and think that this could be interesting to some evolutionary biologist who is trying to find a niche subject to publish articles about. However, neoteny has a far wider and more important reach in the biological literature than a curious evolutionary trick for several reasons
a) Some biologists argue that neotenic development played an important role in the development of our own species. (Subject of a future post)
b) It is more widespread with various consequences in the animal kingdom
c) Neoteny offers answers to some cases of rapid speciation and phenotypical changes.
In this post I will focus on neoteny in general and add some thoughts.
I want to stay as a child forever!
One must be careful about what they wish. Nature might grant your request. Neotenous adult is a specimen that has reached sexual maturity and has stopped growing (or transformation) . Conceivably this could happen in two ways:
1- The somatic growth slows down (entirely or partially), the individual reaches sexual maturity and by the time hormones order the growth to stop the individual is sexually mature but has retained some juvenile characteristics.
2 – The somatic growth is unaltered (or relatively less affected) and sexual maturity arrives earlier. By the time the individual is sexually mature and has stopped growing it has retained some juvenile characteristics.
Both ways have been observed. In most mammals neotenous characteristics are a result of slowed down growth. Whereas amphibian neoteny is usually caused by sexual maturity reached before the metamorphosis is completed to adulthood. This generally results in tadpole like adults with gills and permanent aquatic life.
|Bichon Frise: Toy dogs exhibit extremely neotenous characteristics|
|Axolotl: Do not let the looks deceive you|
In amphibians the effects are more dramatic. The lovely creature axolotl (many love to make pets out of them) looks like a fish or overgrown tadpole with small feet. It lives in water, breathes oxygen ,in water (tadpole gills are different from fish gills but they do the same job), and swims like a fish. But, technically, axolotl is a salamander. Its closest cousins complete their metamorphosis and grow lungs, breathe air and live on land as much as in water.
In fact with the right chemical cocktail you can grow an axolotl to a salamander. (2) Unfortunately, because the genes for creating and controlling the adult form have been out of the selection game random mutations have deformed them enough to make the metamorphosed axolotl viable. Chemically awakened axolotl dies.
Why is it an important topic?
Toy dogs and salamanders are fun to look at, and they might be even interesting to do research on. However, the real importance of neotenous development lies elsewhere. Neoteny can explain why some speciation and phenotypical changes happen lightning fast.
One important limitation of evolution through natural selection is that it is slow. Mutations that increase the inclusive fitness of the organism tend to increase in frequency in the population. However, this means that most (virtually all) mutations are very small changes in the genome. Because a more drastic genotypical change is very unlikely to cause beneficial phenotypical changes. Such mega mutations are so statistically improbable that we can safely ignore them.
Of course, large phenotypical effects do not always require mega mutations. Some examples include centipedes and insects. Embryology of these creatures hinge on repeated segments. Insects develop three body parts by manipulating three segments : head, throax, abdomen. Relatively few genes can manipulate the segments. (E.g. a relatively simple mutation causes the fruit fly Drosophilia melanogaster to grow legs instead of antennae. In fact, an absence or suppression of two genes causes this mutation. Suggesting that the default option is to grow legs and antennae have to be grown by the onset or activation of genes acting on the head segment of the insect).
But we are going astray. Let's focus on mega mutations on mammals. We know that mega mutations are so rare that we can ignore them much less trust them to thrust evolution forward (well I cannot resist making this remark. But, evolution, of course, has no preset direction or goal). But natural selection has found a way to walk around the prohibitive odds of mega mutations to induce drastic changes in the phenotype. Yes, we are talking about neoteny!
The reason mega mutations are so rare is because usually mega changes in the body require mega changes in the genome. However, as Richard Dawkins frequently uses the analogy, the relationship of the genome to the body is more like a recipe to a cake than a blueprint to a building. The genome does not give you a stripped down, scaled, 2D version of the body. Genes describe successive steps of protein synthesis which in turn turns the zygote into an adult. If you must change the adult characteristic you have to alter various steps along the way. Both pre-natal and post-natal. Here we enter the wonderful and woefully complex world of embryology. Maybe another post might focus on the subject but for now it should suffice to state that causing a profound change in the adult phenotype requires much meddling at the embryo stage. Because it is very improbable that all genes that must me mutated to allow the necessary change mutate at the same time, in the required direction, mega mutations are very very very rare. But, does that mean mega phenotypical changes are impossible in mammals, fish, or other vertebrates? Well, no. And neoteny provides one of the detours. A way to cause mega phenotype changes without mega mutations.
Now imagine that there is a selection pressure for bigger brains with more plasticity (I.e learning capacity). Now imagine that you have to change the adult chimpanzee's brain into a homo sapiens brain. (Do I really have to point to the fact that I am using the chimpanzee and not the common ancestor – whose looks we have no idea about- for ease of presentation and narration? I would be disappointed if someone drops a comment about how “we do not come from chimpanzees”)
You'd have to rewire a lot of brain, no?
Now imagine that you take the baby chimp brain (and skull) which is larger in proportion and ready to learn new tricks, slow down the somatic growth of the body and end up with a more flexible large brain in an adult body.
This would take a relatively simple mutation that governs growth hormones and puberty.
Well this is too simplistic an illustration to do justice to the neotenous development of human brain. But a task that looks almost impossible (or one that would take a long long time, even in evolutionary time scales) suddenly looks probable.
In later posts, I will explore the neotenous human traits and try to figure out (read: paraphrase research that has already been done by others) to what extent we are grown up babies.