Pinpointing the “Accident” That Let Multicellular Life Evolve

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Are we the result of a genetic accident 600 million years ago or a creative act of God about 6,000 years ago? Has “molecular time travel” revealed the answer?

Many people enjoy tracing their family tree. And while genealogy has been important to people throughout recorded history, the advent of modern genetics has added a new dimension to the pursuit of our roots. We know, for instance, that modern humans have a bit of Neanderthal floating about in their DNA! But do we have a single-celled creature at the deepest root of our family tree? Now a group of evolutionary scientists claims they have resurrected ancient proteins and revealed—through the marvels of molecular time travel—the happy accident that jump-started multicellular life 600 million years ago.

The Glue That Holds Us Together

Our bodies are made of trillions of cells. But what holds those cells together? What keeps them so nicely organized, preventing us from dissolving into a bucket of goo? An important part of that answer is a protein complex that, during cell division, acts like a scaffold to properly orient a cell’s internal components to its surroundings. During cell division, chromosomes are organized on a “mitotic spindle.” Part of the “spindle-scaffolding” complex, a protein called Dlg, like a tiny carabiner, links the mitotic spindle to a molecular marker near the cell’s surface. Thus this important protein enables new cells to be team players, cooperative parts of the tissues to which they belong.1

University of Oregon biochemist Ken Prehoda and colleagues wanted to discover how these scaffolding proteins, which are found in many different animals,2 evolved. He believes his team has, using ancestral protein reconstruction, traced this key component in evolution’s multicellular mystery back to its molecular mother.

Generating Genealogy To Match Phylogeny

The evolutionary story that supposedly shows how different organisms are related to each other is called phylogeny. “Understanding the historical process of protein evolution begins with a phylogeny,” Prehoda’s team writes.3 With this end in mind, the biochemists first determined the amino acid sequence of scaffolding proteins from a variety of animals. After completing this bit of observational science, they moved into the realm of historical speculation based on their evolutionary presuppositions. They created a computer-generated genealogy to connect the evolutionary dots between scaffolding proteins from various animals on the evolutionary tree of life. Then they were able to simulate how the molecular mother of them all might have looked.

To be sure their hypothetical ancestral protein would still function, they synthesized the DNA sequence corresponding to its amino acid sequence and used cultured cells from a fruit fly to manufacture the protein. Upon testing, they found that the synthetic “ancestral” protein functioned just like all the spindle-scaffolding proteins thought to have descended from it. Furthermore, they found, at the base of the flagellum in a unicellular organism, a protein with a very similar structure but a somewhat different function. “It's just coincidence that the two molecules look so similar,” says Joe Thornton, also a senior author of the project and the person who pioneered the techniques for reconstructing ancient proteins through hypothetical evolutionary pathways. “But that lucky resemblance is why a simple genetic event could cause the evolution of a molecular partnership that is now essential to the biology of complex animals.”4

Prehoda and colleagues believe a single ancient mutation got the animal side of multicellular life off the ground.

That unicellular creature, a choanoflagellate, uses its version of the spindle- scaffolding protein to orient itself to other choanoflagellates when forming a sponge-like colony. And because many evolutionists believe sponges were the first multicellular animals to evolve, these scientists believe the basal body protein of the choanoflagellate was the evolutionary biochemical ancestor of the spindle-scaffolding proteins found in all multicellular animals.

Molecules behave the way they do because of their structure. For instance, the properties of the amino acids in a protein cause it to fold into the shape required for it to work properly. On the surface of a spindle-scaffolding protein is an amino acid sequence that binds it to the marker molecule near a cell’s surface. Prehoda’s team noticed that the amino acid sequence in this region almost matches one on an energy-transferring enzyme common to all living cells.5 The simple substitution of just one of these amino acids deactivates the enzyme but gives the molecule a binding site like that on the spindle-scaffolding protein. Therefore, Prehoda and colleagues believe a single ancient mutation got the animal side of multicellular life off the ground.

Shape Shifting for “Easy Evolution”

“How does a protein that performs one task evolve to perform another? And how do complex systems like those that allow cells to work together in an organized way, evolve the many different proteins they require? Our work suggests that new protein functions can evolve with a very small number of mutations. In this case, only one was required,” Prehoda explains. “This mutation is one small change that dramatically altered the protein's function, allowing it to perform a completely different task. You could say that animals really like these proteins because there are now over 70 of them inside of us.”6 Thus, in the supposed transformation of an ancient enzyme into a scaffolding protein, Prehoda believes his team has discovered “a striking model for the evolution of novel molecular functions.”7

The evolutionary scientists maintain that an ancient choanoflagellate’s enzyme-coding gene was first accidentally duplicated. Then they believe a substitution mutation in the spare copy changed the enzyme’s shape. Biochemically this structural change would inhibit the enzymatic function but lock open a hinge-like region to produce a spindle-scaffolding protein. This “historical hinge substitution,”8 presumably opened the door for all sorts of multicellular possibilities. Thus a fortuitous shape-shifting event, they write, “set the stage for the easy evolution of a novel molecular complex and, in turn, a cellular function that now plays an important role in the complex biology of multicellular animals.”9

Mutations are random changes in genetic material. They may be inconsequential, or they may radically alter the structure or function of a gene’s product. We see, for instance, in sickle-cell anemia that a single mutation causes hemoglobin molecules to twist the red blood cells that carry them into a sickle shape irritating to tiny blood vessels. Mutations may destroy existing genetic information. They may even alter the way existing genetic information is expressed, as we have discussed, for instance, in “De-Regulation of an Existing Trait” and “Evolution of Snake Venom: A New Use for Old Genes?” But mutations have not been shown to create new genetic information such as that needed to produce a new kind of organism. Mutations are not the agents or engines of molecules-to-man evolution. They are not the stepping-stones to “easy evolution.”

They think mutations represent stepwise changes that add up to new, increasingly complex information.

Nevertheless, evolutionists typically interpret small differences between the genes of very different sorts of organisms as mutations. They think mutations represent stepwise changes that add up to new, increasingly complex information. And they therefore believe genetic differences between different kinds of organisms enable them to map their ancestral evolutionary relationships.

Thornton believes that because a computer simulation can trace a path for the evolution of complexity through a series of small steps, biological organisms actually are able to evolve that way. He says, “Our experiments show how biological complexity can evolve though simple, high-probability genetic paths. Before the last common ancestor of all animals, when only single-celled organisms existed on Earth, just one tiny change in DNA sequence caused a protein to switch from its primordial role as an enzyme to a new function that became essential to organize multicellular structures.”10 Believing that the biomolecular similarities and differences between organisms are signposts documenting an evolutionary past, Thornton adds, “We hope that the approach we used—reconstructing in detail the ancient history of protein functions—can be applied to the evolution of other key cellular processes, revealing the whole picture of multicellular life evolving from single-celled ancestors.”11

But genetic differences can only be the result of mutations if they occur in organisms that actually are related to each other. And since experimental biology has never shown the genetic mechanism for how one kind of organism can actually evolve into a completely different kind of organism but only vary within each created kind, differences between the genes or proteins of different kinds of organisms cannot be the result of mutations.

Here a single, critically important difference between the two proteins in view is responsible for distinctly different functions, and, thanks to this difference, each performs its function very well. One of the proteins is an energy transfer enzyme common to almost all organisms, and the other is the scaffolding type of protein found in the basal body of single-celled colonial flagellates. Things that are different are not the same, and it is only an unverifiable evolutionary worldview that interprets their sequence similarity as evidence of an ancestral evolutionary relationship through a common ancestor. This small but significant difference in amino acid sequence is best understood, rather, as the result of God’s original design.

Time Travel and Tumor Formation

What about what ScienceDaily calls “molecular time travel”?12 Has Prehoda’s computer taken us “back in time”13 to see what an ancestral molecule looked like? Evolutionary scientists wishfully call this process “ancestral protein reconstruction” But can “resurrected proteins” reveal life’s ancient mysteries? No, they cannot. All the computer did was simulate how a sequence of mutations might theoretically produce a series of similar molecules that are present in organisms at various points on the presumptive evolutionary tree of life. But the ability to simulate something on a computer—even using a straightforward series of genuine chemical reactions—is not evidence that the simulated sequence of mutations happened in real life, much less that it could fuel the upward evolution of complexity. The millions of years of evolution “observed” through “molecular time travel” are as fictional as time travel in the science fiction television programs and books many of us enjoy.

If anything, this work has shed a bit of light on a common design that God used in many kinds of animals and in man to make our multicellular existence possible.

Furthermore, in their effort to discover how multicellular animals, and ultimately people, came to exist, Prehoda and colleagues think they’ve learned information that might be helpful for cancer researchers. Why? Well, cancer cells cease to function as “team players” and embark on a road of unbridled individuality and unrestrained reproduction. Thus their behavior in some ways resembles unicellular organisms more than that of multicellular ones. Cancer cells are not, however, reverting to an evolutionary past, for there is no such past. It is simply that without a properly oriented spindle to align them with each other, dividing cells can form a misshapen tumor instead of the tissue they are supposed to form. Any discovery that sheds light on the molecular processes that distinguish multicellular from unicellular organisms and govern their behavior could be a useful tool in the hands of cancer researchers. But that usefulness has absolutely nothing to do with molecules-to-man evolution.

Prehoda’s team has perhaps added to our understanding of how multicellular life is possible and how it differs from unicellular life, despite some biochemical similarities. But it has not revealed how multicellular life came to exist. If anything, this work has shed a bit of light on a common design that God used in many kinds of animals and in man to make our multicellular existence possible.

Further Reading

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2016 Volume 11


  1. As Prehoda and colleagues explain, “To form and maintain organized tissues, multicellular organisms orient their mitotic spindles relative to neighboring cells. A molecular complex scaffolded by the GK protein-interaction domain (GKPID) mediates spindle orientation in diverse animal taxa by linking microtubule motor proteins to a marker protein on the cell cortex localized by external cues.” Prehoda’s team sought to “illuminate how this complex evolved and commandeered control of spindle orientation from a more ancient mechanism.” From Douglas P. Anderson et al., “Evolution of an Ancient Protein Function Involved in Organized Multicellularity in Animals,” eLife (January 7, 2016): 1, accessed February 6, 2016, doi: 10.7554/eLife.10147.
  2. Prehoda’s team of biochemists has not yet confirmed that this sort of protein complex really is present in all animals, but they believe the fact that it serves the same function “in multiple cell types in both protostomes and deuterostomes suggests an ancient and essential role in the biology of complex animals.” They admit that “further work is required to comprehensively assess the generality of the GKPID complex’s role in spindle orientation across cell types and in the most basal animal lineages.” From Anderson et al., “Evolution of an Ancient Protein Function Involved in Organized Multicellularity in Animals,” 2.
  3. Anderson et al., “Evolution of an Ancient Protein Function Involved in Organized Multicellularity in Animals,” 4.
  4. University of Chicago Medical Center, “Team Identifies Ancient Mutation That Contributed to Evolution of Multicellular Animals,” ScienceDaily, January 7, 2016,
  5. Five amino acids differ.
  6. University of Oregon, “Random Mutation, Protein Changes, Tied to Start of Multicellular Life,” ScienceDaily, January 7, 2016,
  7. Anderson et al., “Evolution of an Ancient Protein Function Involved in Organized Multicellularity in Animals,” 3.
  8. Ibid., 13.
  9. Ibid., 14.
  10. University of Chicago Medical Center, “Team Identifies Ancient Mutation That Contributed to Evolution of Multicellular Animals.”
  11. Ibid.
  12. University of Oregon, “Random Mutation, Protein Changes, Tied to Start of Multicellular Life.”
  13. Tanya Lewis, “We Might Not Exist If Not for This Accident That Happened 600 Million Years Ago,” Science Alert, January 12, 2016,


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