Rosa Rubicondior: Refuting Creationism - A Tiny Piece of DNA That's So Unkind To Creationists

Saturday, 16 August 2025

Refuting Creationism - A Tiny Piece of DNA That's So Unkind To Creationists

A Genetic Twist that Sets Humans Apart

Humans and chimpanzees share about 98–99% of their DNA, so the vast differences between us must lie within that small fraction where we differ.

Humans have no organs or structures that chimpanzees don’t also have; the differences are mainly in relative size and proportion. In other words, they’re quantitative, not qualitative. But that doesn’t stop creationists solemnly declaring that we are a totally different “kind” — a human “kind” — while chimps are lumped with gorillas, bonobos, and orangutans into the “ape kind.” Two bins, job done.

Creationists insist that no “kind” could have evolved from another because that would require brand-new organs and “new genetic information,” something they claim is impossible. Instead, they set up a straw man, accusing scientists of believing new genes and structures simply pop into existence out of thin air, like some sort of Darwinian magic trick, while insisting no one can explain how it works. (Apparently, gene duplication, mutation, and selection don’t count when you’ve decided in advance that the answer must be wrong.)

But when it comes to humans and chimpanzees, their reasoning ties itself in knots. Humans can’t have evolved from a chimp-like ancestor, they say, because that would be “macro-evolution.” Except when it isn’t. Lions, tigers, leopards, cheetahs, and house cats are all just one happy “cat kind,” because in that case there was obviously no “macro-evolution” — only “variation.” So, if evolution produces cats, that’s “micro-evolution.” If it produces humans, it’s “macro-evolution,” and therefore impossible. Heads I win, tails you lose.

In reality, the major differences between humans and chimpanzees aren’t about inventing new bits and pieces, but in how the same components developed. The key lies in relative sizes of bones, muscles, and teeth — and above all in the brain: not new parts, but differences in growth, proportion, and how the brain is wired.

Now, researchers at the University of California San Diego School of Medicine have shown that part of that small genetic difference — specifically a stretch of DNA called HAR123 — acts as an enhancer controlling brain growth and development. In other words, the real evolutionary leap wasn’t the conjuring up of brand-new organs from nowhere, but changes in how existing genes fine-tuned brain development. The decisive shift came not from what parts the brain has, but from how large they grew and the ratio of cell types — glial cells and neurons — within them.

What are HARs?

Human Accelerated Regions (HARs) are stretches of the human genome that are highly conserved across vertebrates (meaning they’ve stayed almost unchanged for millions of years) but show unusually rapid evolution in humans.
In other words, compared to chimpanzees, gorillas, mice, and other mammals, these regions are almost identical — except in humans, where they’ve picked up a striking number of mutations in a relatively short evolutionary timescale.
About 3,000 HARs have been identified. Most of them are not genes themselves but regulatory DNA (enhancers or silencers) that control when and where genes are switched on.

Why are HARs important?

Because they’re so conserved elsewhere, changes in HARs are thought to have had big functional effects in humans.
Many HARs are active during embryonic development, particularly in the developing brain, influencing neural growth, connectivity, and cortical expansion.
HARs are therefore prime suspects in explaining why human brains are so different from those of chimpanzees despite the overall 98–99% similarity in DNA.

HAR123 specifically
The UC San Diego study you’re referring to looked at HAR123, one of these regions:

Location/function: HAR123 is an enhancer that regulates genes involved in cerebral cortex development.
Key finding: The human version of HAR123 promotes greater growth of neural progenitor cells than the chimpanzee version. These are stem-like cells that give rise to neurons and glial cells.
Mechanism: In organoid experiments (lab-grown mini-brains), swapping in the human HAR123 sequence altered growth patterns in ways consistent with the larger, more complex human cortex.
Conclusion: The big difference between human and chimpanzee brains is not new brain parts, but changes in regulatory DNA that tweak the balance of neurons and support cells during development.

The bigger picture

HARs collectively support the idea that tiny tweaks in regulatory DNA (rather than “new genes” popping into existence, as creationists caricature it) drove many of the distinctive human traits.
In evolutionary terms, it shows how quantitative changes in gene expression can produce qualitative differences in outcome — a larger, more interconnected brain with different cell ratios.

Human Accelerated Regions (HARs) and the “Specified Information” Gambit

Creationists sometimes claim that Human Accelerated Regions (HARs) are “specified genetic information” and therefore evidence of design. In fact, the reality is the exact opposite.

HARs are not new instructions written from scratch. They are stretches of DNA that have been conserved across vertebrates for millions of years, but in humans have accumulated small mutations more quickly than expected. These are tweaks to existing sequences, not brand-new code dropped in from nowhere.
The changes are the product of mutation and selection. Random mutations occur all the time; most are neutral or harmful, but some turn out to have advantages. In the case of HAR123 and others, the mutations altered how much, when, or where nearby genes are expressed — particularly during brain development.
“Specified information” is just a rhetorical label. The “specification” in HARs is nothing mystical — it’s simply the outcome of ordinary evolutionary processes fine-tuning regulatory DNA. Calling this “design” is like calling erosion “designed landscaping.”
Design isn’t needed to explain the pattern. HARs fit evolutionary expectations perfectly: highly conserved regions stay stable because changes are usually harmful, but in a lineage under new selective pressures (like hominin brain expansion), a handful of mutations that alter growth rates can spread. That’s exactly what the evidence shows.

In other words, HARs are not evidence of an intelligent designer scribbling “new information” into our genome. They are textbook examples of how evolution works: tiny changes in regulatory DNA producing profound differences over time.

Their findings are detailed in a paper in Science Advances and summarised in a UC San Diego news release.

A Genetic Twist that Sets Humans Apart
Humans are 99% genetically identical to chimpanzees — how does the other 1% make us different?
Research from scientists at University of California San Diego School of Medicine have shed new light on an age-old question: what makes the human brain unique?

The team’s discovery comes from their investigation of human-accelerated regions (HARs) — sections of the human genome that have accumulated an unusually high level of mutations as humans have evolved. There is a lot of scientific interest in HARs, as they are hypothesized to play an essential role in conferring human-specific traits, and also have links to neurodevelopmental disorders, such as autism.

One reason why scientists think that HARs confer human-specific traits is because they have undergone rapid changes in their genetic sequences since we split from our closest living relative—the chimpanzee—approximately 5 million years ago.

Now, UC San Diego researchers have identified one particular HAR—called HAR123—that appears to be instrumental in shaping the human brain.

The researchers found:

HAR123 itself is not a gene, but is instead a type of molecular “volume control" known as a transcriptional enhancer. Transcriptional enhancers control which genes are activated, how much they are activated, and at what times they are activated during an organism’s development.
Through its role as a transcriptional enhancer, HAR123 promotes the development of neural progenitor cells, the cells that give rise to the two main types of brain cells — neurons and glial cells.
HAR123 also influences the ratio of neurons and glial cells that form from neural progenitor cells.

Ultimately, HAR123 promotes a particularly advanced human trait called cognitive flexibility, or the ability to unlearn and replace previous knowledge.

In addition to providing new insights into the biology of the human brain, the results also offer a molecular explanation for some of the radical changes that have occurred in the human brain over the course of our evolution. This is supported, for example, by the authors’ finding that the human version of HAR123 exerts different molecular and cellular effects than the chimpanzee version in both stem cells and neuron precursor cells in a petri dish.

Further research is needed to more fully understand the molecular action of HAR123 and whether the human version of HAR123 does indeed confer human-specific neural traits. This line of research could lead us to a better understanding of the molecular mechanisms underlying many neurodevelopmental disorders, such as autism.

The study, published online in Science Advances, was led by Miles Wilkinson, Ph.D., distinguished professor, and Kun Tan, Ph.D., assistant professor, both within the Department of Obstetrics, Gynecology, & Reproductive Sciences at UC San Diego School of Medicine. Wilkinson is also affiliate faculty of the UC San Diego Institute for Genomic Medicine. The study was funded, in part, by grants from the National Institutes of Health and 10x Genomics. The authors declare no competing interests.

Publication:
Kun Tan et al.
An ancient enhancer rapidly evolving in the human lineage promotes neural development and cognitive flexibility. Sci. Adv. 11, eadt0534 (2025). DOI:10.1126/sciadv.adt0534

Abstract
The genetic changes driving the evolution of humans since the human-chimpanzee split have been elusive. Here, we report a promising candidate in a chromosomal region linked with neurological defects—17p13.3. We show that this 442-nucleotide sequence—human-accelerated region (HAR) 123—is a conserved neural enhancer that promotes neural progenitor cell (NPC) formation. While present in all mammals, HAR123 has rapidly evolved since humans diverged from chimpanzees. The human and chimpanzee HAR123 orthologs exhibit subtle differences in their neural developmental effects, and the human HAR123 ortholog uniquely regulates many genes involved in neural differentiation. We identified direct targets of the HAR123 enhancer and showed that HIC1 acts downstream of HAR123 to promote human NPC formation. HAR123-knockout mice exhibit a defect in cognitive flexibility and a shift in neural-glia ratio in specific regions of the hippocampus. Our study has implications for neurodevelopmental disorders, which are often accompanied by altered neural-glia ratio and have been linked with HARs.

INTRODUCTION
The concept that rapidly evolving human sequences are a major force in driving human evolution was first championed in 2006 (1, 2). Two criteria were used to identify such human-accelerated regions (HARs): (i) strong conservation and (ii) rapid sequence changes selectively in the human lineage. The former strongly implies functionality; the latter raises the possibility of positive selection for unique functions in humans (3). To date, ~3000 HARs have been defined, with an average length of ~260 nucleotides (nt) (4–6). The majority of HARs (96%) reside in noncoding regions (7). Of these noncoding HARs, many are transcriptional enhancers (8–10). A recent study provided evidence that almost half of HARs are enhancers (5).

Little is known about the biological functions of HARs. Most of what we know comes from studies conducted in mice. Using an overexpression approach in transgenic mice, Boyd et al. (10) provided evidence that the human version of the frizzled class receptor 8 (FZD8) enhancer, HARE5, increases neural progenitor cell (NPC) proliferation, promotes cortical size, and promotes neuron density. Dutrow et al. (11) replaced the mouse ortholog of the HAR2 enhancer with its human ortholog and found that this altered the expression of one of its targets, Gbx2, in a manner suggesting that HAR2 has a role in the evolution of limb development. Using the same approach, Aldea et al. (12) showed that En1 candidate enhancer 18 (ECE18), an enhancer that overlaps with HAR 2XHAR20, regulates the expression of the ENGRAILED-1 transcription factor in a species-biased manner, suggesting a role in the formation of eccrine sweat glands, which are present in higher density in humans than chimpanzees. While these studies have been illuminating, the biological roles of these and other HARs remain poorly understood.

In this study, we report the identification of a HAR that functions in the nervous system. We demonstrate neural roles for this HAR, both in vitro and in vivo, and provide evidence that the human version of this HAR confers several properties—both phenotypic and molecular—that differ from the chimpanzee version, raising the possibility that this HAR has played a role in the evolution of human-specific neural traits.

Kun Tan et al.
An ancient enhancer rapidly evolving in the human lineage promotes neural development and cognitive flexibility. Sci. Adv. 11, eadt0534 (2025). DOI:10.1126/sciadv.adt0534

Copyright: © 2025 The authors.
Published by the American Association for the Advancement of Science. Open access.
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)

Human Accelerated Regions like HAR123 beautifully illustrate the contrast between science and creationist dogma. To a scientist, they are evidence of evolution at work: sequences that stayed almost unchanged across countless species suddenly show rapid change in the human lineage, coinciding with the development of our distinctive brain. To a creationist, they are just “mystery DNA” to be waved away as “specified information” and declared proof of a designer — with no testable mechanism offered.

What makes HARs so compelling is that they don’t conjure up “new genes” out of nowhere, as creationists caricature evolution. Instead, they are tweaks to existing regulatory DNA that alter the timing and level of gene activity. In the case of HAR123, these tweaks helped fuel the expansion and wiring of the human brain. Small genetic changes, filtered through natural selection, had large cumulative effects. This is exactly what evolutionary theory predicts.

Creationism, on the other hand, cannot explain why HARs exist at all. Why would a designer painstakingly preserve these sequences unchanged for millions of years in other species, only to suddenly alter them in humans? Why would the mechanism so obviously mimic the patterns expected from mutation and selection? The creationist “kind” model has no answer — unless one counts circular arguments and shifting definitions of “macro” vs “micro” evolution.

In short, HARs are not awkward anomalies for evolution but shining examples of it. They expose creationist claims for what they are: empty rhetoric, collapsing the moment evidence is examined. The difference between humans and chimpanzees is written, not in miraculous new genetic “kinds,” but in the fine-tuning of ancient DNA by ordinary evolutionary processes.

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