Aron Ra has been battling a particularly pretentious creationist who insist that he has evidence for creationism. Here’s the short list of his arguments:

1. Taxonomically Restricted Essential Genes (orphan genes)
2. pervasive molecular convergence
3. upstream development gene regulatory networks cannot be mutated without lethal disturbance

Aron sent me a more thorough summary of his claims that I’ll include below the fold, but it was really a lot of pompous noise from a guy who had been gleaning scientific terms from the creationist literature, which he presented as evidence that refuted evolution and therefore, in creationist illogic, proved creation.

So we had a little dialogue about these claims. It could have been a debate, but the creationist ran away and refused to join the conversation.

The summary from Aron Ra:

I asked this idiot for evidence for his magical creator, what he calls a “common designer”. This was his reply:

“Observed biological facts for common design… Yes.

(1) Taxomonically Restricted Essential Genes (orphan genes),

About that, he said that orphan genes are “100% unique to a specific species, genus, and family”. And that “These genes show strong evidence for separate ancestry. Studies across comparative genomics show that roughly 10% to 20% of the genes in every sequenced organism are orphan genes.” He describes this as contradicting evolution, requiring what he calls a “rescuing device” to maintain belief in evolution, and that rescuing device, he says is “De Novo. This explains how the non-coding random junk DNA spontaneously mutated into functional protein coding genes.”

(2) pervasive molecular convergence (identical codes for echolocation, digestive enzymes, prestin in unrelated organisms),

About that, he said that “Finding a stable, novel enzyme fold by chance in unguided sequence space (1 in 10^77 functional space) is statistically and chemically equivalent to an unguided physical impossibility.” And that “Whenever identical complex genetic machinery or identical gene-breakage patterns (like GULO across primates, bats, guinea pigs, and birds) contradict a single evolutionary tree, universal common descent invokes unguided “convergent evolution” over and over.”

“The motor protein Prestin produces identical acoustic high-frequency amino acid convergence between echolocating bats and toothed whales, grouping them together ahead of other mammals on a raw molecular tree.”

“Phylogenetic trees rely on common ancestry as an unchallengeable null hypothesis, dismissing conflicting sequence data (like Prestin) as “convergence” and treating human intra-species genealogy tools (PMC12336972) as proof of macroevolutionary transitions across phyla.”

And (3) upstream development gene regulatory networks cannot be mutated without lethal disturbance.”

About that, he said that: “In modern laboratories, altering upstream dGRN kernels causes developmental catastrophe and embryonic lethality. Postulating that ancient unguided mutations somehow rewired core developmental kernels without causing lethality appeals to an unobserved, untestable exception to developmental biology.”

“In molecular biology, core replication origins and transcriptional complexes operate under strict biochemical constraints. Eukaryotic and prokaryotic machineries are non-exchangeable, requiring dual-origin shuttle vectors during cloning. Even within mammals, regulatory sequences of ribosomal RNA genes exhibit strict species-specific promoter-polymerase barriers; human RNA Polymerase I transcription factors cannot properly recognize mouse rDNA promoter elements, and vice versa.”

“transitioning between fundamentally different body plans (such as non-bilaterian to bilaterian, or invertebrates to vertebrates) requires the origin of novel, tightly integrated developmental Gene Regulatory Networks (dGRNs) and taxonomically restricted (“orphan”) genes with unique protein-coding structures.”

“Constructing the chordate architecture (notochord, dorsal nerve cord, pharyngeal arches) requires a distinct, tightly integrated set of upstream dGRN kernels. As Eric Davidson demonstrated, core kernels cannot be altered in developing embryos without causing developmental catastrophe. Moving downstream switches (such as FGF4 retrogenes in Dachshunds) explains minor limb scaling within an established family, but operational science provides no mutational mechanism showing how the upstream chordate regulatory kernels arose from a non-chordate ancestor.”

His conclusion is that “Common design accounts for the empirical evidence we observe daily: modular regulatory switches that permit rapid, robust horizontal diversification within kinds, accompanied by hard developmental and reproductive boundaries, lineage-specific orphan genes, and deep structural constraints that resist unguided transformation.”

https://www.youtube.com/live/FaUZ-e188tE

In addition to all of that, he also said that “evolutionary biologists claimed 98% of the human genome was junk DNA. Only 1% to 2% of human DNA codes for proteins. The rest were evolutionary leftovers.” But then he said that “in 2012, ENCODE published papers that 80% of the human genome is biologically active and functional. In a famous 2013 paper titled “On the Immortality of Television Sets”, evolutionary biologists Dan Grair wrote: “If the ENCODE functional capacity is 80% then evolution is false”. To keep evolution intact, the functional part of the genome had to be less than 10-15%. They shifted to “well, transcription doesn’t mean function, most of that activity is useless cellular noise, so junk still exists”. This “noise” continues to shrink with regulatory roles for non-coding DNA regions and uncovering other functions. And the rescuing device in this case was mostly co-option.”

And finally, he said that “fossil succession is disparity preceding diversity.” And that “Phylum-level architectures appear abruptly, followed only by sub-lineage pruning and variation.”

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If we have time, we may also cover the following:

“Kinds are defined by reproductive compatibility and hybridization limits, aligning generally with the family level (Canidae, Felidae, Equidae). Distinct species within these families readily interbreed to form viable hybrids, while cross-family breeding between distinct body plans does not occur.
This boundary is real and testable:”

“I appreciate you consulting Professor PZ Myers, though it is telling that a university biologist opened a scientific critique with vulgar schoolyard insults (“What a wanker,” “bullshit”). Setting the bluster aside, what was his substantive answer to my question on how the upstream chordate dGRN kernels originated from a non-chordate ancestor? He noted that fruit flies use Brachyury homologs in gut invagination while chordates use Brachyury in notochord formation, concluding they were “readily co-opted into the GRN for notochord formation… so we know where, when, and how notochords evolved.” Declaring that a master transcription factor was “readily co-opted” is not a demonstrated mutational mechanism; it is evolutionary teleology. In fruit flies, mutating that pathway halts gastrulation. By what demonstrated mutational steps does an unguided process rewire an essential endodermal gut-formation program into an axial mesodermal rod without causing embryonic lethality during gastrulation in the intermediate organisms?
Myers didn’t cite a mutational pathway; he pointed to a shared protein family and declared the problem solved by co-option. Reusing identical modular parts across different biological platforms is the hallmark of common systems engineering.
Furthermore, Myers cited Di Gregorio’s work on cis-regulatory modules (CRMs). As Eric Davidson explicitly defined, CRMs and differentiation gene batteries are peripheral, downstream switches – the exact switches I have repeatedly noted allow terminal variation. Di Gregorio himself conceded the “lack of self-evident linear conservation between the cis-regulatory regions identified in Ciona and those identified in other chordates.” Shuffling downstream transcription factor binding sites does not demonstrate how the core upstream kernels that establish the chordate body plan assembled.”

“This exchange has confirmed the real impasse. When pressed on hard developmental genetics:
– PZ Myers pointed to fruit fly gut genes being “readily co-opted” into chordate notochords; a storytelling narrative, not an observed mutational mechanism.
– Eric Davidson’s documented embryonic lethality regarding core dGRN kernels remains unbridged by unguided mutations.
– The existence of Taxonomically Restricted Essential Genes (orphans) remains unexplained by gradual duplication and divergence.
– The mathematical search across sequence space (1 in 10^77) remains an impassable combinatorial barrier for unguided mechanisms.
Universal common descent relies on historical storytelling, computational tree assumptions, and an endless array of ad-hoc rescuing devices to preserve a single tree.”

He specifically said “genetic markers do not confirm ancestry”.

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Evolution can also explain away more contradictory results, the orphan genes (100% unique to a specific species, genus, and family). These genes show strong evidence for separate ancestry. Studies across comparative genomics show that roughly 10% to 20% of the genes in every sequenced organism are orphan genes. And, we have a rescuing device for this as well: De Novo. This explains how the non-coding random junk DNA spontaneously mutated into functional protein coding genes.