Does Old-Earth Creationism Make God Deceptive?


By Fazale Rana – July 17, 2019

“Are [vestigial structures] unequivocal evidence of evolution?

No. Are they reasonable evidence of evolution? Yes.

Ditto gene sequences.

Appearance of evolution is no more a valid deflection [for the overwhelming evidence for evolution] than the appearance of age is a valid dodge of the overwhelming confluence of evidence of antiquity.

Both are sinking ships. I got off before going under with you on this one.”

—Hill R. (a former old-earth creationist who now espouses theistic evolution/evolutionary creationism)

Most people who follow my work at Reasons to Believe know I question the grand claim of the evolutionary paradigm; namely, that evolutionary processes provide the exclusive explanation for the origin, design, and history of life. In light of my skepticism, friends and foes alike often ask me how I deal with (what many people perceive to be) the compelling evidence for the evolutionary history of life, such as vestigial structures and shared genetic features in genomes.

As part of my response, I point out that this type of evidence for evolution can be accommodated by a creation model, with the shared features reflecting common design, not common descent—particularly now that we know that there is a biological rationale for many vestigial structures and shared genetic features. This response prompted my friend Hill R. to level his objection. In effect, Hill says I am committing the “appearance of evolution” fallacy, which he believes is analogous to the “appearance of age” fallacy committed by young-earth creationists (YECs).

Hill is not alone in his criticism. Other people who embrace theistic evolution/evolutionary creation (such as my friends at BioLogos) level a similar charge. According to these critics, both appearance of age and appearance of evolution fallacies make God deceptive.

If biological systems are designed, but God made them appear as if they evolved, then the conclusions we draw when we investigate nature are inherently untrustworthy. This is a problem because, according to Scripture, God reveals himself to us through the record of nature. But if we are misled by nature’s features and, consequently, draw the wrong conclusion, then it makes God deceptive. However, God cannot lie or deceive. It is contrary to his nature.

So, how do I respond to this theological objection to RTB’s creation model?

Before I reply, I want to offer a little more background information to make sure that anyone who is unfamiliar with this concern can better appreciate the seriousness of the charge against our creation model. If you don’t need the background explanation, then feel free to skip ahead to A Response to the Appearance of Evolution Challenge.

Evidence for Evolution: Vestigial Structures

Evolutionary biologists often point to vestigial structures—such as the pelvis and hind limbs of whales and dolphins (cetaceans)—as compelling evidence for biological evolution. Evolutionary biologists view vestigial structures this way because they are also homologous (structurally similar) structures. Vestigial structures are rudimentary body parts that are smaller and simpler than the corresponding features possessed by the other members of a biological group. As a case in point, the whale pelvis and hind limbs are homologous to the pelvis and hind limbs of all other mammals.


Figure 1: Whale Pelvis. Image credit: Shutterstock

Evolutionary biologists believe that vestigial structures were fully functional at one time but degenerated over the course of many generations because the organisms no longer needed them to survive in an ever-changing environment—for example, when the whale ancestor transitioned from land to water. From an evolutionary standpoint, fully functional versions of these structures existed in the ancestral species. The structures’ form and function may be retained (possibly modified) in some of the evolutionary lineages derived from the ancestral species, but if no longer required, the structures become diminished (and even lost) in other lineages.

Evidence for Evolution: Shared Genetic Features

Evolutionary biologists also consider shared genetic features found in organisms that naturally group together as compelling evidence for common descent. One feature of particular interest is the identical (or nearly identical) DNA sequence patterns found in genomes. According to this line of reasoning, the shared patterns arose as a result of a series of substitution mutations that occurred in the common ancestor’s genome. Presumably, as the varying evolutionary lineages diverged from the nexus point, they carried with them the altered sequences created by the primordial mutations.

Synonymous mutations play a significant role in this particular argument for common descent. Because synonymous mutations don’t alter the amino acid sequence of proteins, their effects are considered to be inconsequential. (In a sense, they are analogous to vestigial anatomical features.) So, when the same (or nearly the same) patterns of synonymous mutations are observed in genomes of organisms that cluster together into the same group, most life scientists interpret them as compelling evidence of the organisms’ common evolutionary history.

A Response to the Evidence for Evolution

As a rejoinder to this evidence, I point out that we continue to uncover evidence that vestigial structures display function (see Vestigial Structures are Functional in the Resources section.) Likewise, evidence is beginning to accumulate that synonymous mutations have functional consequences. (see Shared Genetic Features Reflect Design in the Resources section.) Again, if these features have functional utility, then they can reasonably be interpreted as the Creator’s handiwork.

But, even though these biological features bear function, many critics of the RTB model think that the shared features of these biological systems still bear the hallmarks of an evolutionary history. Therefore, they argue that these features look as if they evolved. And if so, we are guilty of the “appearance of evolution” fallacy.

Appearance of Age and the Appearance of Evolution

In 1857, Philip Gosse, a biologist and preacher from England, sought to reconcile the emerging evidence for Earth’s antiquity with Scripture. Gosse was convinced that the earth was old. He was also convinced that Scripture taught that the earth was young. In an attempt to harmonize these disparate stances, he proposed the appearance of age argument in a book titled Omphalos. In this work, Gosse argued that God created Earth in six days, but made it with the appearance of age.


Figure 2: Philip Henry Gosse, 1855. Image credit: Wikipedia

This idea persists today, finding its way into responses modern-day YECs make to the scientific evidence for Earth’s and life’s antiquity. For many people (including me), the appearance of age argument is fraught with theological problems, the chief one being that it makes God deceptive. If Earth appears to be old, and it measures to be old, yet it is young, then we can’t trust anything we learn when we study nature. This problem is not merely epistemological; it is theological because nature is one way that God has chosen to make himself known to us. But if our investigation of nature is unreliable, then it means that God is untrustworthy.

In other words, on the surface, both the appearance of age and the appearance of evolution arguments made by YECs and old-earth creationists (OECs), respectively, seem to be equally problematic.

But does the RTB position actually commit the appearance of evolution fallacy? Does it suffer from the same theological problems as the argument first presented by Gosse in Omphalos? Are we being hypocritical when we criticize the appearance of age fallacy, only to commit the appearance of evolution fallacy?

A Response to the Appearance of Evolution Challenge

This charge against the RTB creation model neglects to fully represent the reasons I question the evolutionary paradigm.

First, my skepticism is not theologically motivated but scientifically informed. For example, I point out in an article I recently wrote for Sapientia that a survey of the scientific literature makes it clear that evolutionary theory as currently formulated cannot account for the key transitions in life’s history, including:

  • the origin of life
  • the origin of eukaryotic cells
  • the origin of body plans
  • the origin of human exceptionalism

Additionally, some predictions that flow out of the evolutionary paradigm have failed (such as the widespread prevalence of convergence), further justifying my skepticism. (See Scientific Challenges to the Evolutionary Paradigm in the Resources section.)

In other words, when we interpret shared features as a manifestation of common design (including vestigial structures and shared genetic patterns), it is in the context of scientifically demonstrable limitations of the evolutionary framework to fully account for life’s origin, history, and design. To put it differently, because of the shortcomings of evolutionary theory, we don’t see biological systems as having evolved. Rather, we think they’ve been designed.

Appearance of Design Fallacy

Even biologists who are outspoken atheists readily admit that biological and biochemical systems appear to be designed. Why else would Nobel Laureate Francis Crick offer this word of caution to scientists studying biochemical systems: “Biologists must keep in mind that what they see was not designed, but rather evolved.”1 What other reason would evolutionary biologist Richard Dawkins offer for defining biology as “the study of complicated things that give the appearance of having been designed for a purpose”?2

Biologists can’t escape the use of design language when they describe the architecture and operation of biological systems. In and of itself, this practice highlights the fact that biological systems appear to be designed, not evolved.

To sidestep the inexorable theological implications that arise when biologists use design language, biologist Colin Pittendrigh coined the term teleonomy in 1958 to describe systems that appear to be purposeful and goal-directed, but aren’t. In contrast with teleology—which interprets purposefulness and goal-directedness as emanating from a Mind— teleonomy views design as the outworking of evolutionary processes. In other words, teleonomy allows biologists to utilize design language— when they describe biological systems—without even a tinge of guilt.

In fact, the teleonomic interpretation of biological design resides at the heart of the Darwinian revolution. Charles Darwin claimed that natural selection could account for the design of biological systems. In doing so, he supplanted Mind with mechanism. He replaced teleology with teleonomy.

Prior to Darwin, biology found its grounding in teleology. In fact, Sir Richard Owen—one of England’s premier biologists in the early 1800s—produced a sophisticated theoretical framework to account for shared biological features found in organisms that naturally cluster together (homologous structures). For Owen (and many biologists of his time) homologous structures were physical manifestations of an archetypal design that existed in the Creator’s mind.

Thus, shared biological features—whether anatomical, physiological, biochemical, or genetic—can be properly viewed as evidence for common design, not common descent. In fact, when Darwin proposed his theory of evolution, he appropriated Owen’s concept of the archetype but then replaced it with a hypothetical common ancestor.

Interestingly, Owen (and other like-minded biologists) found an explanation for vestigial structures like the pelvis and hind limb bones (found in whales and snakes) in the concept of the archetype. They regarded these structures as necessary to the architectural design of the organism. In short, a model that interprets shared biological characteristics from a design/creation model framework has historical precedence and is based on the obvious design displayed by biological systems.

Given the historical precedence for interpreting the appearance of design in biology as bona fide design and the inescapable use of design language by biologists, it seems to me that RTB’s critics commit the appearance of design fallacy when they (along with other biologists) claim that things in biology look designed, but they actually evolved.

Theories Are Underdetermined by Data

A final point. One of the frustrating aspects of scientific discovery relates to what’s called the underdetermination thesis.3 Namely, two competing theories can explain the same set of data. According to this idea, theories are underdetermined by data. This limitation means that two or more theories—that may be radically different from one another—can equally account for the same data. Or, to put it another way, the methodology of science never leads to one unique theory. Because of this shortcoming, other factors—nonscientific ones—influence the acceptance or rejection of a scientific theory, such as a commitment to mechanistic explanations to explain all of biology.

As a consequence of the underdetermination theory, evolutionary models don’t have the market cornered when it comes to offering an interpretation of biological data. Creation models, such as the RTB model—which relies on the concept of common design—also makes sense of the biological data. And given the inability of current evolutionary theory to explain key transitions in life’s history, maybe a creation model approach is the better alternative.

In other words, when we interpret vestigial structures and shared genetic features from a creation model perspective, we are not committing an appearance of age type of fallacy, nor are we making God deceptive. Instead, we are offering a common sense and scientifically robust interpretation of the elegant designs so prevalent throughout the living realm.

Far from a sinking ship one should abandon, a creation model offers a lifeline to scientific and biblical integrity.


Vestigial Structures Are Functional

Shared Genetic Features Reflect Design

Scientific Challenges for the Evolutionary Paradigm

Archetype Biology

  1. Francis Crick, What Mad Pursuit: A Personal View of Scientific Discovery (New York: Basic Books, 1988), 138.
  2. Richard Dawkins, The Blind Watchmaker: Why the Evidence for Evolution Reveals a Universe without Design (New York: W. W. Norton, 1996), 4.
  3. Val Dusek, Philosophy of Technology: An Introduction (Malden, MA: Blackwell Publishing, 2006), 12.

Reprinted with permission by the author

Original article at:

Membrane Biochemistry Challenges Route to Evolutionary Origin of Complex Cells


By Fazale Rana – July 10, 2019

Unfortunately, the same thing could be said to biologists trying to discover the evolutionary route that led to the emergence of complex, eukaryotic cells. No matter the starting point, it seems as if you just can’t get there from here.

This frustration becomes most evident as evolutionary biologists try to account for the biochemical makeup of the membranes found in eukaryotic cells. In my opinion, this struggle is not just an inconvenient detour. As the following paragraphs show, obstacles line the roadway, ultimately leading to a dead end that exposes the shortcomings of the endosymbiont hypothesis—a cornerstone idea in evolutionary biology.

Endosymbiont Hypothesis

Most biologists believe that the endosymbiont hypothesis stands as the best explanation for the origin of complex cells. According to this hypothesis, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe.

The mitochondrion represents the “poster child” of the endosymbiont hypothesis. Presumably, this organelle started as an endosymbiont. Evolutionary biologists believe that once engulfed by the host cell, the microbe took up permanent residency, growing and dividing inside the host. Over time, the endosymbiont and host became mutually interdependent, with the endosymbiont providing a metabolic benefit—such as a source of ATP—for the host cell. In turn, the host cell provided nutrients to the endosymbiont. Presumably, the endosymbiont gradually evolved into an organelle through a process referred to as genome reduction. This reduction resulted when genes from the endosymbiont’s genome were transferred into the genome of the host organism.

Evidence for the Endosymbiont Hypothesis
1. Most of the evidence for the endosymbiont hypothesis centers around mitochondria and their similarity to bacteria. Mitochondria are about the same size and shape as a typical bacterium and have a double membrane structure like gram-negative cells. These organelles also divide in a way that is reminiscent of bacterial cells.

2. Biochemical evidence also exists for the endosymbiont hypothesis. Evolutionary biologists view the presence of the diminutive mitochondrial genome as a vestige of this organelle’s evolutionary history. They see the biochemical similarities between mitochondrial and bacterial genomes as further evidence for the evolutionary origin of these organelles.

3. The presence of the unique lipid, cardiolipin, in the mitochondrial inner membrane also serves as evidence for the endosymbiont hypothesis. This important lipid component of bacterial inner membranes is not found in the membranes of eukaryotic cells—except for the inner membranes of mitochondria. In fact, biochemists consider it a signature lipid for mitochondria and a vestige of the organelle’s evolutionary history. So far, the evolutionary route looks well-paved and clear.

Discovery of Lokiarchaeota

Evolutionary biologists have also developed other lines of evidence in support of the endosymbiont hypothesis. For example, biochemists have discovered that the genetic core (DNA replication and the transcription and translation of genetic information) of eukaryotic cells resembles that of the archaea. This similarity suggests to many biologists that a microbe belonging to the archaeal domain served as the host cell that gave rise to eukaryotic cells.

Life scientists think they may have determined the identity of that archaeal host. In 2015, a large international team of collaborators reported the discovery of Lokiarchaeota, a new phylum belonging to the archaea. This phylum clusters with eukaryotes on the evolutionary tree. Analysis of the genomes of Lokiarchaeota identifies a number of genes involved in membrane-related activities, suggesting that this microbe may well have possessed the ability to engulf other microbes.1 At this point, it looks like “you can get there from here.”

Challenges to the Endosymbiont Hypothesis

Despite this seemingly compelling evidence, the evolutionary route to the first eukaryotic cells is littered with potholes. I have written several articles detailing some of the obstacles. (See Challenges to the Endosymbiont Hypothesis in the Resources section.) Also, a divide on the evolutionary roadway called the lipid divide compounds the problem for the endosymbiont hypothesis.

Lipid Divide

The lipid divide refers to the difference in the chemical composition of the cell membranes found in bacteria and archaea. Phospholipids comprise the cell membranes of both sorts of microbes. But the similarity ends there. The chemical makeup of the phospholipids is distinct in bacteria and archaea.

Bacterial phospholipids are built around a d-glycerol backbone, which has a phosphate moiety bound to the glycerol in the sn-3 position. Two fatty acids are bound to the d-glycerol backbone at the sn-1 and sn-2 positions. In water, these phospholipids assemble into bilayer structures.


Figure: Difference between archaeal (top) and bacterial (middle and bottom) phospholipids. Features include 1: isoprene chains, 2: ether linkage, 3: l-glycerol, 4 and 8: phosphate group, 5: fatty acid chains, 6: ester linkages, 7: d-glycerol, 9: lipid bilayer of bacterial membranes, 10: lipid monolayer found in some archaea. Image credit: Wikipedia

Archaeal phospholipids are constructed around an l-glycerol backbone (which produces membrane lipids with different stereochemistry than bacterial phospholipids). The phosphate moiety is attached to the sn-1 position of glycerol. Two isoprene chains are bound to the sn-2 and sn-3 positions of l-glycerol via ether linkages. Some archaeal membranes are formed from phospholipid bilayers, while others are formed from phospholipid monolayers.

Presumably, the structural features of the archaeal phospholipids serve as an adaptation that renders them ideally suited to form stable membranes in the physically and chemically harsh environments in which many archaea find themselves.

Lipid Divide Frustrates the Origin of Eukaryotic Cell Membranes

In light of the lipid divide and the evidence that seemingly indicates that the endosymbiotic host cell likely belonged to Lokiarchaeota, it logically follows that the membrane composition of eukaryotic cells should be archaeal-like. But, this expectation is not met and the evolutionary route encounters another pothole. Instead, the cell membranes of eukaryotic cells closely resemble bacterial membranes.

One way to repair the roadway is to posit that during the evolutionary process that led to the emergence of eukaryotic cells, a transition from archaeal-like membranes to bacterial-like membranes took place. In fact, supporting evidence comes from laboratory studies demonstrating that stable bilayers can form from a mixture of bacterial and archaeal phospholipids, even though the lipids from the two sources have opposite stereochemistry.

Evolutionary biologists Purificación López-García and David Moreira question if evidence can be marshaled in support of this scenario for two reasons.2 First, mixing of phospholipids in the lab is a poor model for cell membranes that function as a “dynamic cell-environment interface.”3

Second, they question if this transition is feasible given how exquisitely optimized membrane proteins must be to fit into cell membranes. The nature of protein optimization is radically different for bacterial and archaeal membranes. Because cell membrane systems are optimized, the researchers question if an adequate driving force for this transition exists.

In other words, these two scientists express serious doubts about the biochemical viability of a transitional stage between archaeal membranes. In light of these obstacles, López-García and Moreira write, “The archaea-to-bacteria membrane shift remains the Achilles’ heel for these models [that propose an archaeal host for endosymbionts].”4

In other words, you can’t get there from here.

Can Lokiarchaeota Traverse the Lipid Divide?

In the midst of this uncertain evolutionary route, a recent study by investigators from the Netherlands seems to point the way toward the evolutionary origin of eukaryotic membranes.5 Researchers screened the Lokiarchaeota genome for enzymes that would take part in phospholipid synthesis with the hope of finding clues about how this transition may have occurred. They conclude that this group of microbes could not make l-glycerol-1-phosphate (a key metabolic intermediate in the production of archaeal phospholipids) because it lacked the enzyme glycerol-1-phosphate dehydrogenase (G1PDH). They also discovered evidence that suggests that this group of microbes could make fatty acids and chemically attach them to sugars. The researchers argue that Lokiarchaeota could make some type of hybrid phospholipid with features of both archaeal and bacterial phospholipids.

The team’s approach to understanding how evolutionary processes could bridge the lipid divide and account for the origin of eukaryotic membranes is clever and inventive, to be sure. But it is far from convincing for at least four reasons.

1. Absence of evidence is not evidence of absence, as the old saying goes. Just because the research team didn’t find the gene for G1PDH in the Lokiarchaeota genetic material doesn’t mean this microbe didn’t have the capacity to make archaeal-type phospholipids. Toward this end, it is important to note that researchers have not cultured any microbe that belongs to this group organisms. The group’s existence is inferred from metagenomic analysis, which involves isolating small fragments of DNA from the environment (in this case a hydrothermal vent system in the Atlantic Ocean, called Loki’s Castle) and stitching them together into a genome. The Lokiarchaeota “genome” is low quality (1.4-fold coverage) and incomplete (8 percent of the genome is missing). Around one-third (32 percent) of the genome codes for proteins with unknown function. Could it be that an enzyme capable of generating l-glycerol-1-phosphate exists in the mysterious third of the genome? Or in the missing 8 percent?

2. While the researchers discovered that genes could conceivably work together to make d-glycerol-3-phosphate (though the enzymes encoded by these genes perform different metabolic functions), they found no direct evidence that Lokiarchaeota produces d-glycerol-3-phosphate. Nor did they find evidence for glycerol-3-phosphate dehydrogenase (G3PDH) in the Lokiarchaeota genetic material. This enzyme plays a key role in the synthesis of phospholipids in bacteria.

3. Though the researchers found evidence that Lokiarchaeota had the capacity to make fatty acids, some of the genes required for the process seem to have been acquired by these microbes via horizontal gene transfer with genetic material from bacteria. (It should be noted that 29 percent of the Lokiarchaeota genome comes from the bacteria.) It is not clear when Lokiarchaeota acquired these genes and, therefore, if this metabolic capability has any bearing on the origin of eukaryotes.

4. The researchers present no evidence that Lokiarchaeota possessed the protein machinery that would chemically attach isoprenoid lipids to d-glycerol-3-phosphate via ether linkages.

Thus, the only way to establish Lokiarchaeota membranes as a transitional evolutionary pathway between those found in Archaea and Bacteria is to perform chemical analysis of its membranes. At this juncture, such analysis is impossible to perform because no one has been able to culture Lokiarchaeota. In fact, other evidence suggests that this group of microbes possessed archaeal-type membranes. Researchers have recovered archaeal lipids in the sediments surrounding Loki’s Castle, but they have not recovered bacterial-like lipids.

More Lipid Divide Frustration

Given these problems, could it be that the host microbe for the endosymbiont was a member of Bacteria, not Archaea? While this model would solve the problem of the lipid divide, it leaves unexplained the similarity between the genetic core of eukaryotes and the Archaea. Nor does it account for the grouping of eukaryotes with the Archaea.

It doesn’t look like you can get there from here, either.

Evolutionary biologists Jonathan Lombard, Purificación López-García and David Moreira sum things up when they write, “The origin of eukaryotic membranes is a problem that is rarely addressed by the different hypotheses that have been proposed to explain the emergence of eukaryotes.”6 Yet, until this problem is adequately addressed, the evolutionary route to eukaryotes will remain obscure and the endosymbiont hypothesis noncompelling.

In light of this challenge and others, maybe a better way to make sense of the origin of eukaryotic cells is to view them as the Creator’s handiwork. For many scientists, it is a road less traveled, but it accounts for all of the data. You can get there from here.


Challenges to the Endosymbiont Hypothesis

Support for a Creation Model for the Origin of Eukaryotic Cells

  1. Anja Spang et al., “Complex Archaea that Bridge the Gap between Prokaryotes and Eukaryotes,” Nature 521 (May 14, 2015): 173–79, doi:10.1038/nature14447; Katarzyna Zaremba-Niedzwiedzka et al., “Asgard Archaea Illuminate the Origin of Eukaryotic Cellular Complexity,” Nature 541 (January 19, 2017): 353–58, doi:10.1038/nature21031.
  2. Purificación López-García and David Moreira, “Open Questions on the Origin of Eukaryotes,” Trends in Ecology and Evolution 30, no. 11 (November 2015): 697–708, doi:10.1016/j.tree.2015.09.005.
  3. López-García and Moreira, “Open Questions.”
  4. López-García and Moreira, “Open Questions.”
  5. Laura Villanueva, Stefan Schouten, and Jaap S. Sinninghe Damsté, “Phylogenomic Analysis of Lipid Biosynthetic Genes of Archaea Shed Light on the ‘Lipid Divide,’” Environmental Microbiology 19, no. 1 (January 2017): 54–69, doi:10.1111/1462-2920.13361.
  6. Jonathan Lombard, Purificación López-García, and David Moreira, “The Early Evolution of Lipid Membranes and the Three Domains of Life,” Nature Reviews Microbiology 10 (June 11, 2012): 507–15, doi:10.1038/nrmicro2815.

Reprinted with permission by the author

Original article at:

Satellite DNA: Critical Constituent of Chromosomes

Untitled 4

By Fazale Rana – June 26, 2019

Let me explain.

Recently, I wound up with a disassembled cabinet in the trunk of my car. Neither my wife Amy nor I could figure out where to put the cabinet in our home and we didn’t want to store it in the garage. The cabinet had all its pieces and was practically new. So, I offered it to a few people, but there were no takers. It seemed that nobody wanted to assemble the cabinet.

Getting Rid of the Junk

After driving around with the cabinet pieces in my trunk for a few days, I channeled my inner Marie Kondo. This cabinet wasn’t giving me any joy by taking up valuable space in the trunk. So, I made a quick detour on my way home from the office and donated the cabinet to a charity.

When I told Amy what I had done, she expressed surprise and a little disappointment. If she had known I was going to donate the cabinet, she would have kept it for its glass doors. In other words, if I hadn’t donated the cabinet, it would have eventually wound up in our garage because it has nice glass doors that Amy thinks she could have repurposed.

There is a point to this story: The cabinet was designed for a purpose and, at one time, it served a useful function. But once it was disassembled and put in the trunk of my car, nobody seemed to want it. Disassembling the cabinet transformed it into junk. And since my wife loves to repurpose things, she saw a use for it. She didn’t perceive the cabinet as junk at all.

The moral of my little story also applies to the genomes of eukaryotic organisms. Specifically, is it time that evolutionary scientists view some kinds of DNA not as junk, but rather as purposeful genetic elements?

Junk in the Genome

Many biologists hold the view that a vast proportion of the genomes of other eukaryotic organisms is junk, just like the disassembled cabinet I temporarily stored in my car. They believe that, like the unwanted cabinet, many of the different types of “junk” DNA in genomes originated from DNA sequences that at one time performed useful functions. But these functional DNA sequences became transformed (like the disassembled cabinet) into nonfunctional elements.

Evolutionary biologists consider the existence of “junk” DNA as one of the most potent pieces of evidence for biological evolution. According to this view, junk DNA results when undirected biochemical processes and random chemical and physical events transform a functional DNA segment into a useless molecular artifact. Junk pieces of DNA remain part of an organism’s genome, persisting from generation to generation as a vestige of evolutionary history.

Evolutionary biologists highlight the fact that, in many instances, identical (or nearly identical) segments of junk DNA appear in a wide range of related organisms. Frequently, the identical junk DNA segments reside in corresponding locations in these genomes—and for many biologists, this feature clearly indicates that these organisms shared a common ancestor. Accordingly, the junk DNA segment arose prior to the time that the organisms diverged from their shared evolutionary ancestor and then persisted in the divergent evolutionary lines.

One challenging question these scientists ask is, Why would a Creator purposely introduce nonfunctional, junk DNA at the exact location in the genomes of different, but seemingly related, organisms?

Satellite DNA

Satellite DNA, which consists of nucleotide sequences that repeat over and over again, is one class of junk DNA. This highly repetitive DNA occurs within the centromeres of chromosomes and also in the chromosomal regions adjacent to centromeres (referred to as pericentromeric regions).


Figure: Chromosome Structure. Image credit: Shutterstock

Biologists have long regarded satellite DNA as junk because it doesn’t encode any useful information. Satellite DNA sequences vary extensively from organism to organism. For evolutionary biologists, this variability is a sure sign that these DNA sequences can’t be functional. Because if they were, natural selection would have prevented the DNA sequences from changing. On top of that, molecular biologists think that satellite DNA’s highly repetitive nature leads to chromosomal instability, which can result in genetic disorders.

A second challenging question is, Why would a Creator intentionally introduce satellite DNA into the genomes of eukaryotic organisms?

What Was Thought to Be Junk Turns Out to Have Purpose

Recently, a team of biologists from the University of Michigan (UM) adopted a different stance regarding the satellite DNA found in pericentromeric regions of chromosomes. In the same way that my wife Amy saw a use for the cabinet doors, the researchers saw potential use for satellite DNA. According to Yukiko Yamashita, the UM research head, “We were not quite convinced by the idea that this is just genomic junk. If we don’t actively need it, and if not having it would give us an advantage, then evolution probably would have gotten rid of it. But that hasn’t happened.”1

With this mindset—refreshingly atypical for most biologists who view satellite DNA as junk—the UM research team designed a series of experiments to determine the function of pericentromeric satellite DNA.2 Typically, when molecular biologists seek to understand the functional role of a region of DNA, they either alter it or splice it out of the genome. But, because the pericentromeric DNA occupies such a large proportion of chromosomes, neither option was available to the research team. Instead, they made use of a protein found in the fruit fly Drosophila melanogaster, called D1. Previous studies demonstrated that this protein binds to satellite DNA.

The researchers disabled the gene that encodes D1 and discovered that fruit fly germ cells died. They observed that without the D1 protein, the germ cells formed micronuclei. These structures reflect chromosomal instability and they form when a chromosome or a chromosomal fragment becomes dislodged from the nucleus.

The team repeated the study, but this time they used a mouse model system. The mouse genome encodes a protein called HMGA1 that is homologous to the D1 protein in fruit flies. When they damaged the gene encoding HMGA1, the mouse cells also died, forming micronuclei.

As it turns out, both D1 and HMGA1 play a crucial role, ensuring that chromosomes remain bundled in the nucleus. These proteins accomplish this feat by binding to the pericentromeric satellite DNA. Both proteins have multiple binding sites and, therefore, can simultaneously bind to several chromosomes at once. The multiple binding interactions collect chromosomes into a bundle to form an association site called a chromocenter.

The researchers aren’t quite sure how chromocenter formation prevents micronuclei formation, but they speculate that these structures must somehow stabilize the nucleus and the chromosomes housed in its interior. They believe that this functional role is universal among eukaryotic organisms because they observed the same effects in fruit flies and mice.

This study teaches us two additional lessons. One, so-called junk DNA may serve a structural role in the cell. Most molecular biologists are quick to overlook this possibility because they are hyper-focused on the informational role (encoding the instructions to make proteins) DNA plays.

Two, just because regions of the genome readily mutate without consequences doesn’t mean these sequences aren’t serving some kind of functional role. In the case of pericentromeric satellite DNA, the sequences vary from organism to organism. Most molecular biologists assume that because the sequences vary, they must not be functionally important. For if they were, natural selection would have prevented them from changing. But this study demonstrates that DNA sequences can vary—particularly if DNA is playing a structural role—as long as they don’t compromise DNA’s structural utility. In the case of pericentromeric DNA, apparently the nucleotide sequence can vary quite a bit without compromising its capacity to bind chromocenter-forming proteins (such as D1 and HMGA1).

Is the Evolutionary Paradigm the Wrong Framework to Study Genomes?

Scientists who view biology through the lens of the evolutionary paradigm are often quick to conclude that the genomes of organisms reflect the outworking of evolutionary history. Their perspective causes them to see the features of genomes, such as satellite DNA, as little more than the remnants of an unguided evolutionary process. Within this framework, there is no reason to think that any particular DNA sequence element harbors function. In fact, many life scientists regard these “evolutionary vestiges” as junk DNA. This clearly was the case for satellite DNA.

Yet, a growing body of data indicates that virtually every category of so-called junk DNA displays function. In fact, based on the available data, a strong case can be made that most sequence elements in genomes possess functional utility. Based on these insights, and the fact that pericentromeric satellite DNA persists in eukaryotic genomes, the team of researchers assumed that it must be functional. It’s a clear departure from the way most biologists think about genomes.

Based on this study (and others like it), I think it is safe to conclude that we really don’t understand the molecular biology of genomes.

It seems to me that we live in the midst of a revolution in our understanding of genome structure and function. Instead of being a wasteland of evolutionary debris, the architecture and operations of genomes appear to be far more elegant and sophisticated than anyone ever imagined—at least within the confines of the evolutionary paradigm.

This insight also leads me to wonder if we have been using the wrong paradigm all along to think about genome structure and function. I contend that viewing biological systems as the Creator’s handiwork provides a superior framework for promoting scientific advance, particularly when the rationale for the structure and function of a particular biological system is not apparent. Also, in addressing the two challenging questions, if biological systems have been created, then there must be good reasons why these systems are structured and function the way they do. And this expectation drives further study of seemingly nonfunctional, purposeless systems with the full anticipation that their functional roles will eventually be uncovered.

Though committed to an evolutionary interpretation of biology, the UM researchers were rewarded with success when they broke ranks with most evolutionary biologists and assumed junk regions of the genome were functional. Their stance illustrates the power of a creation model approach to biology.

Sadly, most evolutionary biologists are like me when it comes to old furniture. We lack vision and are quick to see it as junk, when in fact a treasure lies in front of us. And, if we let it, this treasure will bring us joy.


  1. University of Michigan, “Scientists Discover a Role for ‘Junk’ DNA,” ScienceDaily (April 11, 2018),
  2. Madhav Jagannathan, Ryan Cummings, and Yukiko M. Yamashita, “A Conserved Function for Pericentromeric Satellite DNA,” eLife 7 (March 26, 2018): e34122, doi:10.7554/eLife.34122.

Endosymbiont Hypothesis and the Ironic Case for a Creator



i ·ro ·ny

The use of words to express something different from and often opposite to their literal meaning.
Incongruity between what might be expected and what actually occurs.

—The Free Dictionary

People often use irony in humor, rhetoric, and literature, but few would think it has a place in science. But wryly, this has become the case. Recent work in synthetic biology has created a real sense of irony among the scientific community—particularly for those who view life’s origin and design from an evolutionary framework.

Increasingly, life scientists are turning to synthetic biology to help them understand how life could have originated and evolved. But, they have achieved the opposite of what they intended. Instead of developing insights into key evolutionary transitions in life’s history, they have, ironically, demonstrated the central role intelligent agency must play in any scientific explanation for the origin, design, and history of life.

This paradoxical situation is nicely illustrated by recent work undertaken by researchers from Scripps Research (La Jolla, CA). Through genetic engineering, the scientific investigators created a non-natural version of the bacterium E. coli. This microbe is designed to take up permanent residence in yeast cells. (Cells that take up permanent residence within other cells are referred to as endosymbionts.) They hope that by studying these genetically engineered endosymbionts, they can gain a better understanding of how the first eukaryotic cells evolved. Along the way, they hope to find added support for the endosymbiont hypothesis.1

The Endosymbiont Hypothesis

Most biologists believe that the endosymbiont hypothesis (symbiogenesis) best explains one of the key transitions in life’s history; namely, the origin of complex cells from bacteria and archaea. Building on the ideas of Russian botanist Konstantin Mereschkowski, Lynn Margulis(1938–2011) advanced the endosymbiont hypothesis in the 1960s to explain the origin of eukaryotic cells.

Margulis’s work has become an integral part of the evolutionary paradigm. Many life scientists find the evidence for this idea compelling and consequently view it as providing broad support for an evolutionary explanation for the history and design of life.

According to this hypothesis, complex cells originated when symbiotic relationships formed among single-celled microbes after free-living bacterial and/or archaeal cells were engulfed by a “host” microbe. Presumably, organelles such as mitochondria were once endosymbionts. Evolutionary biologists believe that once engulfed by the host cell, the endosymbionts took up permanent residency, with the endosymbiont growing and dividing inside the host.

Over time, the endosymbionts and the host became mutually interdependent. Endosymbionts provided a metabolic benefit for the host cell—such as an added source of ATP—while the host cell provided nutrients to the endosymbionts. Presumably, the endosymbionts gradually evolved into organelles through a process referred to as genome reduction. This reduction resulted when genes from the endosymbionts’ genomes were transferred into the genome of the host organism.


Figure 1: Endosymbiont hypothesis. Image credit: Wikipedia.

Life scientists point to a number of similarities between mitochondria and alphaproteobacteria as evidence for the endosymbiont hypothesis. (For a description of the evidence, see the articles listed in the Resources section.) Nevertheless, they don’t understand how symbiogenesis actually occurred. To gain this insight, scientists from Scripps Research sought to experimentally replicate the earliest stages of mitochondrial evolution by engineering E. coli and brewer’s yeast (S. cerevisiae) to yield an endosymbiotic relationship.

Engineering Endosymbiosis

First, the research team generated a strain of E. coli that no longer has the capacity to produce the essential cofactor thiamin. They achieved this by disabling one of the genes involved in the biosynthesis of the compound. Without this metabolic capacity, this strain becomes dependent on an exogenous source of thiamin in order to survive. (Because the E. coli genome encodes for a transporter protein that can pump thiamin into the cell from the exterior environment, it can grow if an external supply of thiamin is available.) When incorporated into yeast cells, the thiamin in the yeast cytoplasm becomes the source of the exogenous thiamin, rendering E. coli dependent on the yeast cell’s metabolic processes.

Next, they transferred the gene that encodes a protein called ADP/ATP translocase into the E. coli strain. This gene was harbored on a plasmid (which is a small circular piece of DNA). Normally, the gene is found in the genome of an endosymbiotic bacterium that infects amoeba. This protein pumps ATP from the interior of the bacterial cell to the exterior environment.2

The team then exposed yeast cells (that were deficient in ATP production) to polyethylene glycol, which creates a passageway for E. coli cells to make their way into the yeast cells. In doing so, E. coli becomes established as endosymbionts within the yeast cells’ interior, with the E. coli providing ATP to the yeast cell and the yeast cell providing thiamin to the bacterial cell.

Researchers discovered that once taken up by the yeast cells, the E. coli did not persist inside the cell’s interior. They reasoned that the bacterial cells were being destroyed by the lysosomal degradation pathway. To prevent their destruction, the research team had to introduce three additional genes into the E. coli from three separate endosymbiotic bacteria. Each of these genes encodes proteins—called SNARE-like proteins—that interfere with the lysosomal destruction pathway.

Finally, to establish a mutualistic relationship between the genetically-engineered strain of E. coli and the yeast cell, the researchers used a yeast strain with defective mitochondria. This defect prevented the yeast cells from producing an adequate supply of ATP. Because of this limitation, the yeast cells grow slowly and would benefit from the E. coli endosymbionts, with the engineered capacity to transport ATP from their cellular interior to the exterior environment (the yeast cytoplasm.)

The researchers observed that the yeast cells with E. coli endosymbionts appeared to be stable for 40 rounds of cell doublings. To demonstrate the potential utility of this system to study symbiogenesis, the research team then began the process of genome reduction for the E. coli endosymbionts. They successively eliminated the capacity of the bacterial endosymbiont to make the key metabolic intermediate NAD and the amino acid serine. These triply-deficient E. coli strains survived in the yeast cells by taking up these nutrients from the yeast cytoplasm.

Evolution or Intentional Design?

The Scripps Research scientific team’s work is impressive, exemplifying science at its very best. They hope that their landmark accomplishment will lead to a better understanding of how eukaryotic cells appeared on Earth by providing the research community with a model system that allows them to probe the process of symbiogenesis. It will also allow them to test the various facets of the endosymbiont hypothesis.

In fact, I would argue that this study already has made important strides in explaining the genesis of eukaryotic cells. But ironically, instead of proffering support for an evolutionary origin of eukaryotic cells (even though the investigators operated within the confines of the evolutionary paradigm), their work points to the necessary role intelligent agency must have played in one of the most important events in life’s history.

This research was executed by some of the best minds in the world, who relied on a detailed and comprehensive understanding of biochemical and cellular systems. Such knowledge took a couple of centuries to accumulate. Furthermore, establishing mutualistic interactions between the two organisms required a significant amount of ingenuity—genius that is reflected in the experimental strategy and design of their study. And even at that point, execution of their experimental protocols necessitated the use of sophisticated laboratory techniques carried out under highly controlled, carefully orchestrated conditions. To sum it up: intelligent agency was required to establish the endosymbiotic relationship between the two microbes.


Figure 2: Lab researcher. Image credit: Shutterstock.

Or, to put it differently, the endosymbiotic relationship between these two organisms was intelligently designed. (All this work was necessary to recapitulate only the presumed first step in the process of symbiogenesis.) This conclusion gains added support given some of the significant problems confronting the endosymbiotic hypothesis. (For more details, see the Resources section.) By analogy, it seems reasonable to conclude that eukaryotic cells, too, must reflect the handiwork of a Divine Mind—a Creator.



  1. Angad P. Mehta et al., “Engineering Yeast Endosymbionts as a Step toward the Evolution of Mitochondria,” Proceedings of the National Academy of Sciences, USA 115 (November 13, 2018): doi:10.1073/pnas.1813143115.
  2. ATP is a biochemical that stores energy used to power the cell’s operation. Produced by mitochondria, ATP is one of the end products of energy harvesting pathways in the cell. The ATP produced in mitochondria is pumped into the cell’s cytoplasm from within the interior of this organelle by an ADP/ATP transporter.
Reprinted with permission by the author
Original article at:

Yeast Gene Editing Study Raises Questions about the Evolutionary Origin of Human Chromosome 2



As a biochemist and a skeptic of the evolutionary paradigm, people often ask me two interrelated questions:

  1. What do you think are the greatest scientific challenges to the evolutionary paradigm?
  2. How do you respond to all the compelling evidence for biological evolution?

When it comes to the second question, people almost always ask about the genetic similarity between humans and chimpanzees. Unexpectedly, new research on gene editing in brewer’s yeast helps answer these questions more definitively than ever.

For many people, the genetic comparisons between the two species convince them that human evolution is true. Presumably, the shared genetic features in the human and chimpanzee genomes reflect the species’ shared evolutionary ancestry.

One high-profile example of these similarities is the structural features human chromosome 2 shares with two chimpanzee chromosomes labeled chromosome 2A and chromosome 2B. When the two chimpanzee chromosomes are placed end to end, they look remarkably like human chromosome 2. Evolutionary biologists interpret this genetic similarity as evidence that human chromosome 2 arose when chromosome 2A and chromosome 2B underwent an end-to-end fusion. They claim that this fusion took place in the human evolutionary lineage at some point after it separated from the lineage that led to chimpanzees and bonobos. Therefore, the similarity in these chromosomes provides strong evidence that humans and chimpanzees share an evolutionary ancestry.


Figure 1: Human and Chimpanzee Chromosomes Compared

Image credit: Who Was Adam? (Covina, CA: RTB Press, 2015), p. 210.

Yet, new work by two separate teams of synthetic biologists from the United States and China, respectively, raises questions about this evolutionary scenario. Working independently, both research teams devised similar gene editing techniques that, in turn, they used to fuse the chromosomes in the yeast species, Saccharomyces cerevisiae (brewer’s yeast).Their work demonstrates the central role intelligent agency must play in end-on-end chromosome fusion, thereby countering the evolutionary explanation while supporting a creation model interpretation of human chromosome 2.

The Structure of Human Chromosome 2

Chromosomes are large structures visible in the nucleus during the cell division process. These structures consist of DNA combined with proteins to form the chromosome’s highly condensed, hierarchical architecture.

yeast-gene-editing-study-2Figure 2: Chromosome Structure

Image credit: Shutterstock

Each species has a characteristic number of chromosomes that differ in size and shape. For example, humans have 46 chromosomes (23 pairs); chimpanzees and other apes have 48 (24 pairs).

When exposed to certain dyes, chromosomes stain. This staining process produces a pattern of bands along the length of the chromosome that is diagnostic. The bands vary in number, location, thickness, and intensity. And the unique banding profile of each chromosome helps geneticists identify them under a microscope.

In the early 1980s, evolutionary biologists compared the chromosomes of humans, chimpanzees, gorillas, and orangutans for the first time.2 These studies revealed an exceptional degree of similarity between human and chimp chromosomes. When aligned, the human and corresponding chimpanzee chromosomes display near-identical banding patterns, band locations, band size, and band stain intensity. To evolutionary biologists, this resemblance reveals powerful evidence for human and chimpanzee shared ancestry.

The most noticeable difference between human and chimp chromosomes is the quantity: 46 for humans and 48 for chimpanzees. As I pointed out, evolutionary biologists account for this difference by suggesting that two chimp chromosomes (2A and 2B) fused. This fusion event would have reduced the number of chromosome pairs from 24 to 23, and the chromosome number from 48 to 46.

As noted, evidence for this fusion comes from the close similarity of the banding patterns for human chromosome 2 and chimp chromosomes 2A and 2B when the two are oriented end on end. The case for fusion also gains support by the presence of: (1) two centromeres in human chromosome 2, one functional, the other inactive; and (2) an internal telomeresequence within human chromosome 2.3 The location of the two centromeres and internal telomere sequences corresponds to the expected locations if, indeed, human chromosome 2 arose as a fusion event.4

Evidence for Evolution or Creation?

Even though human chromosome 2 looks like it is a fusion product, it seems unlikely to me that its genesis resulted from undirected natural processes. Instead, I would argue that a Creator intervened to create human chromosome 2 because combining chromosomes 2A and 2B end to end to form it would have required a succession of highly improbable events.

I describe the challenges to the evolutionary explanation in some detail in a previous article:

  • End-to-end fusion of two chromosomes at the telomeres faces nearly insurmountable hurdles.
  • And, if somehow the fusion did occur, it would alter the number of chromosomes and lead to one of three possible scenarios: (1) nonviable offspring, (2) viable offspring that suffers from a diseased state, or (3) viable but infertile offspring. Each of these scenarios would prevent the fused chromosome from entering and becoming entrenched in the human gene pool.
  • Finally, if chromosome fusion took place and if the fused chromosome could be passed on to offspring, the event would have had to create such a large evolutionary advantage that it would rapidly sweep through the population, becoming fixed.

This succession of highly unlikely events makes more sense, from my vantage point, if we view the structure of human chromosome 2 as the handiwork of a Creator instead of the outworking of evolutionary processes. But why would these chromosomes appear to be so similar, if they were created? As I discuss elsewhere, I think the similarity between human and chimpanzee chromosomes reflects shared design, not shared evolutionary ancestry. (For more details, see my article “Chromosome 2: The Best Evidence for Evolution?”)

Yeast Chromosome Studies Offer Insight

Recent work by two independent teams of synthetic biologists from the US and China corroborates my critique of the evolutionary explanation for human chromosome 2. Working within the context of the evolutionary framework, both teams were interested in understanding the influence that chromosome number and organization have on an organism’s biology and how chromosome fusion shapes evolutionary history. To pursue this insight, both research groups carried out similar experiments using CRISPR/Cas9 gene editing to reduce the number of chromosomes in brewer’s yeast from 16 to 1 (for the Chinese team) and from 16 to 2 (for the team from the US) through a succession of fusion events.

Both teams reduced the number of chromosomes in stages by fusing pairs of chromosomes. The first attempt reduced the number from 16 to 8. In the next round they fused pairs of the newly created chromosome to reduce the number from 8 to 4, and so on.

To their surprise, the yeast seemed to tolerate this radical genome editing quite well—although their growth rate slowed and the yeast failed to thrive under certain laboratory conditions. Gene expression was altered in the modified yeast genomes, but only for a few genes. Most of the 5,800 genes in the brewer’s yeast genome were normally expressed, compared to the wild-type strain.

For synthetic biology, this work is a milestone. It currently stands as one of the most radical genome reconfigurations ever achieved. This discovery creates an exciting new research tool to address fundamental questions about chromosome biology. It also may have important applications in biotechnology.

The experiment also ranks as a milestone for the RTB human origins creation model because it helps address questions about the origin of human chromosome 2. Specifically, the work with brewer’s yeast provides empirical evidence that human chromosome 2 must have been shaped by an Intelligent Agent. This research also reinforces my concerns about the capacity of evolutionary mechanisms to generate human chromosome 2 via the fusion of chimpanzee chromosomes 2A and 2B.

Chromosome fusion demonstrates the critical role intelligent agency plays.

Both research teams had to carefully design the gene editing system they used so that it would precisely delete two distinct regions in the chromosomes. This process affected end-on-end chromosome fusions in a way that would allow the yeast cells to survive. Specifically, they had to delete regions of the chromosomes near the telomeres, including the highly repetitive telomere-associated sequences. While they carried out this deletion, they carefully avoided deleting DNA sequences near the telomeres that harbored genes. They also simultaneously deleted one of the centromeres of the fused chromosomes to ensure that the fused chromosome would properly replicate and segregate during cell division. Finally, they had to make sure that when the two chromosomes fused, the remaining centromere was positioned near the center of the resulting chromosome.

In addition to the high-precision gene editing, they had to carefully construct the sequence of donor DNA that accompanied the CRISPR/Cas9 gene editing package so that the chromosomes with the deleted telomeres could be directed to fuse end on end. Without the donor DNA, the fusion would have been haphazard.

In other words, to fuse the chromosomes so that the yeast survived, the research teams needed a detailed understanding of chromosome structure and biology and a strategy to use this knowledge to design precise gene editing protocols. Such planning would ensure that chromosome fusion occurred without the loss of key genetic information and without disrupting key processes such as DNA replication and chromosome segregation during cell division. The researchers’ painstaking effort is a far cry from the unguided, undirected, haphazard events that evolutionary biologists think caused the end-on-end chromosome fusion that created human chromosome 2. In fact, given the high-precision gene editing required to create fused chromosomes, it is hard to envision how evolutionary processes could ever produce a functional fused chromosome.

A discovery by both research teams further complicates the evolutionary explanation for the origin of human chromosome 2. Namely, the yeast cells could not replicate unless the centromere of one of the chromosomes was deleted at the time the chromosomes fused. The researchers learned that if this step was omitted, the fused chromosomes weren’t stable. Because centromeres serve as the point of attachment for the mitotic spindle, if a chromosome possesses two centromeres, mistakes occur in the chromosome segregation step during cell division.

It is interesting that human chromosome 2 has two centromeres but one of them has been inactivated. (In the evolutionary scenario, this inactivation would have happened through a series of mutations in the centromeric DNA sequences that accrued over time.) However, if human chromosome 2 resulted from the fusion of two chimpanzee chromosomes, the initial fusion product would have possessed two centromeres, both functional. In the evolutionary scenario, it would have taken millennia for one of the chromosomes to become inactivated. Yet, the yeast studies indicate that centromere loss must take place simultaneously with end-to-end fusion. However, based on the nature of evolutionary mechanisms, it cannot.

Chromosome fusion in yeast leads to a loss of fitness.

Perhaps one of the most remarkable outcomes of this work is the discovery that the yeast cells lived after undergoing that many successive chromosome fusions. In fact, experts in synthetic biology such as Gianni Liti (who commented on this work for Nature), expressed surprise that the yeast survived this radical genome restructuring.5

Though both research teams claimed that the fusion had little effect on the fitness of the yeast, the data suggests otherwise. The yeast cells with the fused chromosomes grew more slowly than wild-type cells and struggled to grow under certain culture conditions. In fact, when the Chinese research team cultured the yeast with the single fused chromosome with the wild-type strain, the wild-type yeast cells out-competed the cells with the fused chromosome.

Although researchers observed changes in gene expression only for a small number of genes, this result appears to be a bit misleading. The genes with changed expression patterns are normally located near telomeres. The activity of these genes is normally turned down low because they usually are needed only under specific growth conditions. But with the removal of telomeres in the fused chromosomes, these genes are no longer properly regulated; in fact, they may be over-expressed. And, as a consequence of chromosome fusion, some genes that normally reside at a distance from telomeres find themselves close to telomeres, leading to reduced activity.

This altered gene expression pattern helps explains the slower growth rate of the yeast strain with fused chromosomes and the yeast cells’ difficulty to grow under certain conditions. The finding also raises more questions about the evolutionary scenario for the origin of human chromosome 2. Based on the yeast studies, it seems reasonable to think that the end-to-end fusion of chromosomes 2A and 2B would have reduced the fitness of the offspring that first inherited the fused chromosome 2, making it less likely that the fusion would have taken hold in the human gene pool.

Chromosome fusion in yeast leads to a loss of fertility.

Normally, yeast cells reproduce asexually. But they can also reproduce sexually. When yeast cells mate, they fuse. As a result of this fusion event, the resulting cell has two sets of chromosomes. In this state, the yeast cells can divide or form spores. In many respects, the sexual reproduction of yeast cels resembles the sexual reproduction in humans, in which egg and sperm cells, each with one set of chromosomes, fuse to form a zygote with two sets of chromosomes.


Figure 3: Yeast Cell Reproduction

Image credit: Shutterstock

Both research groups discovered that genetically engineered yeast cells with fused chromosomes could mate and form spores, but spore viability was lower than for wild-type yeast.

They also discovered that after the first round of chromosome fusion when the genetically engineered yeast possessed 8 chromosomes, mating normal yeast cells with those harboring fused chromosomes resulted in low fertility. When wild-type yeast cells were mated with yeast strains that had been subjected to additional rounds of chromosome fusion, spore formation failed altogether.

The synthetic biologists find this result encouraging because it means that if they use yeast with fused chromosomes for biotechnology applications, there is little chance that the genetically engineered yeast will mate with wild-type yeast. In other words, the loss of fertility serves as a safeguard.

However, this loss of fertility does not bode well for evolutionary explanations for the origin of human chromosome 2. The yeast studies indicate that chromosome fusion leads to a loss of fertility because of the mismatch in chromosome number, which makes it difficult for chromosomes to align and properly segregate during cell division. So, why wouldn’t this loss of fertility happen if chromosomes 2A and 2B fuse?


Figure 4: Cell Division

Image credit: Shutterstock

In short, the theoretical concerns I expressed about the evolutionary origin of human chromosome 2 find experimental support in the yeast studies. And the indisputable role intelligent agency plays in designing and executing the protocols to fuse yeast chromosomes provides empirical evidence that a Creator must have intervened in some capacity to design human chromosome 2.

Of course, there are a number of outstanding questions that remain for a creation model interpretation of human chromosome 2, including:

  • Why would a Creator seemingly fuse together two chromosomes to create human chromosome 2?
  • Why does this chromosome possess internal telomere sequences?
  • Why does human chromosome 2 harbor seemingly nonfunctional centromere sequences?

We predict that as we learn more about the biology of human chromosome 2, we will discover a compelling rationale for the structural features of this chromosome, in a way that befits a Creator.

But, at this juncture the fusion of yeast chromosomes in the lab makes it hard to think that unguided evolutionary processes could ever successfully fuse two chromosomes, including human chromosome 2, end on end. Creation appears to make more sense.



  1. Jingchuan Luo et al., “Karyotype Engineering by Chromosome Fusion Leads to Reproductive Isolation in Yeast,” Nature 560 (2018): 392–96, doi:10.1038/s41586-018-0374-x; Yangyang Shao et al., “Creating a Functional Single-Chromosome Yeast,” Nature 560 (2018): 331–35, doi:10.1038/s41586-018-0382-x.
  2. Jorge J. Yunis, J. R. Sawyer, and K. Dunham, “The Striking Resemblance of High-Resolution G-Banded Chromosomes of Man and Chimpanzee,” Science 208 (1980): 1145–48, doi:10.1126/science.7375922; Jorge J. Yunis and Om Prakash, “The Origin of Man: A Chromosomal Pictorial Legacy,” Science 215 (1982): 1525–30, doi:10.1126/science.7063861.
  3. The centromere is a region of the DNA molecule near the center of the chromosome that serves as the point of attachment for the mitotic spindle during the cell division process. Telomeres are DNA sequences located at the tip ends of chromosomes designed to stabilize the chromosome and prevent it from undergoing degradation.
  4. J. W. Ijdo et al., “Origin of Human Chromosome 2: An Ancestral Telomere-Telomere Fusion,” Proceedings of the National Academy of Sciences USA 88 (1991): 9051–55, doi:10.1073/pnas.88.20.9051; Rosamaria Avarello et al., “Evidence for an Ancestral Alphoid Domain on the Long Arm of Human Chromosome 2,” Human Genetics 89 (1992): 247–49, doi:10.1007/BF00217134.
  5. Gianni Liti, “Yeast Chromosome Numbers Minimized Using Genome Editing,” Nature 560 (August 1, 2018): 317–18, doi:10.1038/d41586-018-05309-4.
Reprinted with permission by the author
Original article at: