The nervous system and muscles evolved shortly thereafter.
Zakon gives no citation on this claim. Apparently it is one of evolution’s brute facts which evolutionists need merely to remind themselves of occasionally.
Later Zakon does admit to some problems with the evolutionary tree:
The phylogeny of basal metazoans is poorly resolved, likely because of the rapid radiation of these then-new life forms
So not only did metazoans just happen to arise spontaneously, but they did so in a “rapid radiation.” For every failure of evolutionary theory you can bet there are always the usual explanatory devices competing to fill the gap.
But there’s no getting around nature’s complexities:
in all animals with nervous systems, neurons generate action potentials (APs), release excitatory and inhibitory neurotransmitters, form circuits, receive sensory input, innervate muscle, and direct behavior.
Not bad for something from nothing. As you can see, that just has random mutations written all over it. After all, such molecular engineering marvels just “appear” at some long lost unobservable time and place:
Potassium leak and voltage-dependent K+ (Kv) channels appeared three billion years ago in bacteria and occur in all organisms
Potassium channels “appeared” three billion years ago? For this claim Zakon cites a paper written by evolutionists who presuppose that potassium channels (and everything else for that matter) evolved. In other words, to support his unscientific assertion that potassium channels “appeared” three billion years ago, Zakon cites the work of evolutionists who assume that potassium channels “appeared” at some point.
Just when you thought this evolutionary tale could not become any more bizarre, Zakon explains how he believes these potassium channels “appeared”:
Kv channels are the “founding members” of the family of ion-permeating channels whose basic structure is a protein of six transmembrane helices (6TM) that associate as tetramers to form a channel. At some point early in eukaryote evolution, the gene for a 6TM channel likely duplicated, giving rise to a protein with two domains. These proteins then dimerized to form a complete channel. Such a channel still exists in the two-pore channel family of Ca2+-permeable channels localized in endosomes and lysozomes. The gene for a two domain channel likely duplicated to make a protein with four domains capable of forming a channel on its own (4x6TM). Eventually such a four-domain channel evolved (or retained) permeability to Ca2+, and these handily became involved in intracellular signaling. Other Ca2+-binding proteins and enzymes first appeared in single-celled eukaryotes. Additionally, there are single 6TM Na+-permeable channels in bacteria. Their relationship to eukaryotic [sodium] channels is unclear, and they will not be discussed in this review.
In the world of an evolutionists, astronomically complex structures just happen to form spontaneously. Things appear, duplicate, modify, retain, evolve, serendipitously perform new functions, and so forth.
Zakon goes on to explain that calcium channels also “appear early in animals.” Furthermore, it has been confirmed that sodium channels evolved from calcium channels. And how could evolutionists make such an astonishing discovery? Easy, by comparing the structures and amino acid sequences of these marvels, such as in choanoflagellates:
Analysis of putative Cav and Nav channel genes from fungi, choanoflagellates, and metazoans confirm this speculation and show that choanoflagellates have a channel that groups with recognized [sodium] channels with strong support.
Though they cannot explain how even a single protein could evolve, evolutionists conclude that voltage-gated sodium channels evolved from calcium channels because they share certain similarities.
Later we learn that a variety of key molecular components were luckily finally in place “for construction of the nodes of Ranvier.”
And that electric organs evolved independently in African and American fish as the sodium channel gene “underwent a burst of evolutionary change at the origin of both groups of electric fishes, with numerous substitutions in key regions of the channel.”
Then there are the various neurotoxins, such as tetrodotoxin, that interfere with the sodium channel. Vertebrates that maintain high concentrations of tetrodotoxin must somehow protect their several types of sodium channels from the dangerous poison.
For example, hundreds of fish species, such as the Pufferfish, safely maintain high concentrations of tetrodotoxin with sodium channel genes that have slight differences which help to make the fish immune to tetrodotoxin. But how could these similar differences have evolved in all these different fish species? The slow process of random mutations would require too much time to save a species from its internal poison. Furthermore these modifications would be required in not just one, but all the different sodium channel genes. Once again evolution has an explanatory device:
We still do not know how pufferfish were able to survive with only one or a few tetrodotoxin-resistant [sodium] channels. The most likely scenario is that tetrodotoxin-resistant mutations accumulated gradually in the [sodium] channel genes as fish were initially exposed to a light load of tetrodotoxin. Gradually, as more channels gained resistance, they were able to carry a greater toxic load.
There is always a just-so story.
Then there are the garter snakes and their prey, the newts. Newts maintain high concentrations of tetrodotoxin and garter snakes that eat them have sodium channel genes with the right, immunizing, modifications.
But garter snakes that live in different areas do not have these modifications, and may die if they ingest a newt. In fact it appears that the different garter snakes populations that prey on newts would have had to independently evolve their sodium channel modifications:
Even more striking, tetrodotoxin resistance has evolved multiple times in populations of other species of garter snakes that are also sympatric with newts in the Pacific Northwest and California, as well as other snake species sympatric with other newts or frogs that use tetrodotoxin in South America and Asia.
But that’s not all. The newt larvae do not produce the tetrodotoxin poison but since the adult newts can be cannibalistic the larvae will flee when they smell tetrodotoxin nearby. So in this case tetrodotoxin is a chemical signal. This is also true in pufferfish when males detect nanomolar levels of tetrodotoxin resulting from female egg laying.
This is all fascinating biology and ion channels, such as these voltage-gated sodium channels, are incredible molecular machines. And while it is true that all of this can be explained in a speculative evolutionary narrative, the story here is that, as usual, the biology does not easily fit evolutionary theory. Papers such as this one are cited as yet more confirmations of evolutionary theory, but in fact they are little more than evolutionary story-telling.