Information from Nothing? Darwinists Must Believe It
A minimal cell packs a ton of functional information. How did it get there? Darwinians, who wish to account for all of life without design, are obligated to believe that information creates itself. In the past they tended to be more reticent about the problem, realizing that it was a tremendous challenge even to get to a theoretical replicator. Lately, some of them are employing a bolder tactic: simply assert that information creates itself. Two recent papers in leading journals illustrate the tactic, which often includes extending natural selection down into prebiotic realms where it doesn’t belong.
In Science Magazine, Aaron Wacholder and Anne-Ruxandra Carvunis talk about how to get “new genes from borrowed parts.” In their article, innovation is a key word. It means new information that can perform a function. Where does innovation come from?
The vast phenotypic diversity of life is in part a consequence of a continual process of genetic innovation. New genes, with distinct structures and capabilities, emerge regularly throughout evolutionary history. [Emphasis added.]
There’s the assertion. Innovation emerges. Got it? It just emerges. It emerges regularly. Believe it because we say so.
Making use of genomics technologies, researchers are beginning to form an understanding of the details of the processes by which new genes arise. On page 797 of this issue, Cosby et al. (1) provide clarity for one such process. Transposons are parasitic genomic elements that replicate by inserting copies of themselves in the host genome. Cosby et al. report how vertebrate genes have captured DNA transposon domains, generating new genes that encode new fusion proteins with distinct domain architectures. Fusion of transposon domains with host genes appears to be frequent, with 94 fusion events identified over tetrapod evolution. Transposon domain capture may be a common source of new genes and molecular innovation across the tree of life.
Shuffling Existing Functions
What Rachel Cosby et al. actually demonstrate in their paper in Science is only some minimal kind of “regulatory innovation.” Their method relies on the shuffling of existing functions in transposons when spliced in with genes. This is about as hopeless as getting new meanings from paragraphs from two books that are cut and pasted in random ways.
Our findings confirm that exon shuffling is a major evolutionary force generating genetic novelty. We provide evidence that DNA transposons promote exon shuffling by inserting transposase domains in new genomic contexts. This process provides a plausible path for the emergence of several ancient transcription factors with important developmental functions. By illustrating how a transcription factor and its dispersed binding sites can emerge simultaneously from a single transposon family, our results bolster the view that transposons are key players in the evolution of gene regulatory networks.
The specific example they use is a gene fusion in a certain bat, but they don’t describe a novel function of any significance, like the origin of a bat wing or echolocation. That’s OK with them; just call it a “major evolutionary force generating genetic novelty.” Believe it because they say so.
Although gene birth through duplication has been extensively documented, how novel protein architectures and biological functions are born has remained poorly characterized. Here, we validate that exon shuffling is a major evolutionary force generating genetic novelty, and we provide evidence that DNA transposons fuel the process not only by supplying protein domains to assemble new protein architectures, but also, in many cases, by introducing the splice sites that enable the fusion process. Although these events must be relatively rare on an evolutionary time scale, the mobility of DNA transposons likely increases the probability of generating a functional gene via exon shuffling by introducing genetic material into new contexts.
“Likely” and “Could”
Over and over in the paper, the hedging words “likely” and “could” work to degrade confidence in the assertion. Their only evidence that some new function has emerged is that the changes seem to have been preserved by “purifying selection.” The word information does not even appear in the paper.
The most striking assertions are in a figure in Wachover and Carvunis’s analysis of the paper by Cosby et al., where they showcase six unguided processes behind the “origin of new protein-coding genes.” First are the mechanisms proposed by Cosby et al., including “transposon domain capture” and “gene fusion,” followed by “extreme divergence” and “exon shuffling.” Then they rely on “duplication and divergence” followed by the most audacious claim of all: “de novo birth.” They describe this as “a fully new gene evolves from a previously noncoding sequence.”
In contrast to this class of new gene-formation mechanisms, in which the innovation consists of rearranging functional domains in new contexts, the phenomenon of de novo gene birth from a nongenic sequence generates completely new domains and genes. Although once thought rare, well-characterized cases of de novo gene birth have now been reported in numerous taxa (9).
Reference 9 takes the reader to a paper in PLOS Genetics, co-authored by Carvunis again, where the two authors assert that orphan genes are examples of new genes that appeared out of nowhere! Talk about begging the question. The very evidence that Paul Nelson uses to argue against evolution they use to argue for evolution! Once again, they don’t show any truly wonderful examples like eyes or wings evolving by chance this way. They only define a “function” as something that remains in the genome due to “purifying selection.” Another of their examples of novelty in function is — get this — cancer. Readers can check the open-access paper to see if any of their examples of “de novo genes” really represent information emerging by chance.
Regarding new genes by duplication, Casey Luskin has addressed that claim at length here and here. Ann Gauger and Douglas Axe also addressed the claim in a paper in BIO-Complexity. The bottom line is that blind evolution is oblivious to function. It is not going to store up mutations in a useless strand waiting for it to hit upon some innovation, any more than a duplicated string of letters is going to happen upon some amazing new concept.
Emergent Information at the Origin of Life
Another assertion that information can arise spontaneously is found in a paper in PNAS, by Patrick W. Kudella et al., including Dieter Braun. Like the gene-duplication story, this paper asserts that “Structured sequences emerge from random pool when replicated by templated ligation.” Notice the confident assertions right from the start:
The structure of life emerged from randomness. This is attributed to selection by molecular Darwinian evolution. This study found that random templated ligation led to the simultaneous elongation and sequence selection of oligomers. Product strands showed highly structured sequence motifs which inhibited self-folding and built self-templating reaction networks. By the reduction of the sequence space, the kinetics of duplex formation increased and led to a faster replication through the ligation process. These findings imply that elementary binding properties of nucleotides can lead to an early selection of sequences even before the onset of Darwinian evolution. This suggests that such a simplification of sequence space could result in faster downstream selection for sequence-based function for the origin of life.
It is hard to be charitable to this paper. The authors know full well the problem of error catastrophe for sequences inherited without strict error correction. They also know the vastness of non-functional sequence space. They know that genes are functional not because of repeating structures but because of genetic information. And yet they pursue the worn-out RNA World scenario (see here) with the notion that natural selection might work somehow before accurate replication is available. The brashness of this claim is astonishing:
One of the dominant hypotheses to explain the origin of life is the concept of the RNA world. It is built on the fact that catalytically active RNA molecules can enzymatically promote their own replication via active sites in their three-dimensional structures. These so-called ribozymes have a minimal length of 30 to 41 base pairs and, thus, a sequence space of more than 430 ∼ 1018. The subset of functional, catalytically active sequences in this vast sequence space is vanishingly small, making spontaneous assembly of ribozymes from monomers or oligomers all but impossible.
It’s impossible, but they believe it happened! Such credulity dwarfs the faith of the most deluded cultist. Because they absolutely need some kind of Darwinian selection, they simply assert that it was there: “prebiotic evolution has likely provided some form of selection guiding single nucleotides to form functional sequences and thereby lowering the sequence entropy of this system.” It’s impossible; we need selection; therefore, it must have existed. Huh?
Randomly Ligating Oligonucleotides
Their paper rides on an assumption similar to faith in gene duplication as a source of novelty. They demonstrate that randomly ligating oligonucleotides can form repeating structures. This reduces the entropy, they say, and therefore such structures must be capable of function. Look at what they know are insurmountable hurdles; then look at what they claim must have happened.
For emergence of life on early Earth, oligomers needed to spontaneously show an evolution-like behavior and create structure from randomness. We think this might be difficult for base-by-base replication reactions because of the Eigen error catastrophe. Emerging strands are either accurate copies of the template strand or they become more and more random because of the incorporated errors every time a strand is replicated. Thus, the system loses information and function over time. However, even if the replication fidelity would be below the error threshold and replicated strands were perfect copies of the original strand template, the emergence of a fittest sequence from a random initial pool would require Darwinian selection of function over a potentially very large sequence space.
OK, game over. They can go home now. But wait — there is always faith.
In contrast, we, here, followed templated ligation from a pool of random 12-mer strands made from two bases under temperature oscillations. Both the cooperation of sequences and the usage of ligation instead of base-by-base replication distinguishes this work from ref. 48 and lead to ligated sequences that were highly structured. Those sequences could physically be selected by length using temperature differences. This combination of mechanisms would have a dynamic very similar to Darwinian evolution.
Despite its minimalism, the studied system contains all elements necessary for Darwinian evolution: out of equilibrium conditions, transmission of sequence information from template to substrate strains, reliable reproduction of a subset of oligomer products and the possibility to select from the long fast-growing sequences in the process. At the dawn of life, such pre-Darwinian dynamics would have pushed prebiotic systems toward lower entropy states. A subsequent selection for catalytic function from the replicated structured sequences could then have paved the way toward the eventual emergence of life.
The brashness of evolutionists in believing impossible things by assertion needs some serious shaming. It would be shamed out of court if the dictatorship of the Darwin lobby did not rule science.