Salamanders have their own way of doing things. For most animals, if an important body part, such as a limb, is lost, it is gone for good. But for salamanders, they just grow a new one. Also, salamanders use different embryonic development patterns. For example, their digits (fingers and toes for us humans) form in the wrong order — going, essentially, in the wrong direction.
You can see this from a figure in a paper by Neil Shubin’s group. In the figure, the numbers across the top show the order in which the digits appear. Salamanders go against the common pattern. This “reverse polarity” in what otherwise is a highly conserved development pattern in the tetrapods is a quandary for evolution.
Early evolutionists who first seriously reckoned with this “striking deviance from an otherwise conserved pattern in tetrapods,” as the Shubin paper puts it, as well as other distinctive features of salamander limb development, concluded that the salamanders probably arose independently of the other tetrapods. In other words, these development inconsistencies were so profound they required an independent origin — there were two different origins of tetrapods.
The problem, however, is the set of similarities between the salamanders and their cousin tetrapods is so massive that any such independent origins would be absurd from an evolutionary perspective.
So evolutionists were left needing an explanation for the profound divergence. Perhaps salamanders got their start with a loss of digits. If the first salamanders had only two digits, and then re-evolved the other digits (catching up to their ancestral forms), the development order could have been rearranged.
Unfortunately such a hypothetical evolutionary history, where the salamanders begin by losing digits, does not fit the data (both molecular and fossil) very well, even within the context of evolutionary theory.
Perhaps the salamander digit development deviance arose as a larval adaptation. Or perhaps the salamander development pattern is not a “deviance” at all, but rather is the nominal, ancient pattern, but is retained only in salamanders among living tetrapods.
But these hypotheses have problems as well. In fact the salamander character data are full of contradictions:
The evolution and phylogeny of crown group salamanders is plagued by homoplasy. In fact, a large a number of highly derived anatomical characters, including body elongation, tail autonomy, and life history pathways, have been demonstrated or are debated to have evolved multiple times.
(Note that these anatomical characters have not “been demonstrated” to have evolved multiple times. That is a misrepresentation of the science. They only have “been demonstrated” to have evolved multiple times if one assumes evolution at the outset.)
Yet another problem plaguing these evolutionary hypotheses is the finding of genes unique to the salamander that are crucial for its limb regeneration ability and unique embryonic development patterns. You can read more about these here and here, and this brings us to the second half of our two-fer.
Whether they are called unique genes, novel genes, orphans, ORFans, taxonomically-restricted genes (TRGs), lineage-specific genes (LSGs), or whatever, they are a problem for evolution. First, they counter the above hypotheses attempting to explain the salamander’s unique development. As one paper explains:
[T]he notion of an ancient limb regeneration programme has been challenged by reports of salamander lineage-specific genes (LSGs) upregulated during regeneration. One salamander LSG in particular, the Prod1 gene, was shown to be required for proximodistal patterning during limb regeneration and for ulna, radius and digit formation during forelimb development. The existence of urodele LSGs expressed and involved in regeneration has lent support to the hypothesis that limb regeneration is a derived urodele feature.
In other words, the salamander gets it done using genes unique to its lineage, and that contradicts the hypothesis that the salamander’s unique capabilities were there all along.
It also contradicts the evolutionist’s longstanding, but rapidly fading, hope that ORFans would go away. As I have explained, evolutionists hoped that such lineage-specific genes would be found in other species as more genomes were decoded. But instead the number of ORFans just continued to grow.
Evolutionists next predicted that similar ORFan sequences would be found in the so-called non-coding DNA. Although that is sometimes the case, it is not generally, and the Prod1 gene is another example of this.
Evolutionists next predicted that ORFan sequences were probably not part of a mature protein-coding gene and did not form functional proteins. That also is wrong, and Prod1 is yet another example of an ORFan that is indeed a real protein.
The findings of unique (non-homologous) development patterns, and lineage-specific genes make no sense on evolution. And attempts to explain these findings according to evolution with clever, detailed hypotheses just cause more problems.
If you try to build a house on a faulty foundation, it will just get worse. Evolution is a flawed theory, and the more we learn about biology, the more evident that becomes.