No, These Researchers Did Not See a Single-Celled Organism Evolve Into A Multicellular Organism!

A green algae in a predator-free environment (far left) and other environments with predators. (click for credit)

A student sent me an article from Science Alert, asking me about its rather bold claim:

Scientists Have Witnessed a Single-Celled Algae Evolve Into a Multicellular Organism…Most of us know that at some point in our evolutionary history around 600 million years ago, single-celled organisms evolved into more complex multicellular life. But knowing that happened and actually seeing it happen in real-time in front of you is an entirely different matter altogether. And that’s exactly what researchers from the George Institute of Technology and University of Montana have witnessed – and captured in the breathtaking, time-lapse footage below.

Over the course of my scientific career, I have learned that many science journalists are terrible at science and not much better at journalism, so I did what I always do when I read about science in the popular press: I found the scientific article upon which it was based. Not surprisingly, the study didn’t do what the article claims. It did find one interesting result, however.

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Big News in Epigenetics!

The Grand Prismatic Spring in Yellowstone National Park holds bacteria like the ones in the study being discussed.
(click for credit)

The more we learn about creation, the more it surprises us. While it is true in all areas of science, it seems particularly true in genetics. When I was at university, I was taught as definitive fact that each gene in my DNA determined the makeup of one protein in my body. We now know that is false. I was also taught as definitive fact that the only way a parent can transmit a trait to its offspring is through the sequence of nucleotide bases in DNA. As a result, if a new trait appears in a population, it must be due to a change in the species’ DNA sequence. We now know that is false. For example, I was taught as definitive fact in university that cave fish are blind because of mutations to their DNA. We now know that is false, at least for one species of blind cave fish.

So we now know that there are ways to inherit traits that go beyond the DNA sequence that you inherit from both parents. For example, we know that if you train mice to fear a certain smell, the next generation can inherit that fear. It’s not that the parents train the fear into their offspring (the offspring were raised separate from their trained parent). They actually inherited the fear. How in the world can a parent pass on a fear of something to its offspring? That’s what the field of epigenetics (which literally means “on top of genetics”) wants to find out.

We know that it has something to do with how an organism regulates the activity of its genes. An organism can alter chemical aspects of the DNA that are not related to its actual sequence, and that alteration can decrease the use of a gene, increase the use of a gene, turn a gene off so that it is not used at all, or turn a gene on so that it will start being used. For example, most people are not born lactose intolerant. After all, they drink their mother’s milk or a milk-based formula. Milk digestion requires the enzyme called “lactase,” which is coded for by a gene. While everyone has that gene turned on at birth, in some people, it gets turned off later on, causing lactose intolerance. Nothing has changed in the person’s DNA sequence – the gene is still there and has not been broken. However, that gene has been turned off by epigenetic mechanisms. It is thought that this process is responsible for epigenetic inheritance. To some extent, we must be able to inherit the “off” and “on” status of our parents’ genes.

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Another Failed Evolutionary Prediction

A common fruit fly, Drosophila melanogaster (click for credit)

The acid test of a scientific theory is whether or not it can make testable predictions about things that are not known. If it can’t, it isn’t really a scientific theory. If it can, those predictions should be tested by observation or experiment. If the results of the test confirm the predictions, you can have more faith in the theory. If they do not, you must either alter your theory or abandon it. One of the main reasons I am a creationist is that creationism has made many testable predictions, and many of those predictions have been confirmed. In fact, creationism has a much better track record when it comes to confirmed predictions than does evolution (see here and here).

Recently, I ran across another study that demonstrates another failed prediction of evolutionary theory. It studied the alcohol dehydrogenase protein (ADH) as made by fruit flies. Fruit flies often consume alcohol because they feed on rotting materials, and the ADH they make allows them to do that. How do they make ADH? They have a gene that gives the necessary instructions to the cell. That gene is, in effect, a “recipe” for ADH.

Studies have already shown that the common fruit fly (Drosophila melanogaster) tends to feed on alcohol-rich things (like rotting fruit) more than a similar fruit fly, Drosophila simulans. The evolutionary explanation that has always been given for this fact is that these two fruit flies had a common ancestor, and that ancestor had a gene that made less efficient ADH. As a result, the common ancestor didn’t eat alcohol-rich things.

The evolutionary line that led to the common fruit fly experienced mutations in the ADH gene, and those mutations ended up making the ADH more efficient. Natural selection then caused those fruit flies to survive, because they could now survive by eating a lot of rotting fruit, while the other flies could eat only a little rotting fruit. That process continued over time, eventually leading to the common fruit fly we see today, which eats a lot of rotting fruit. In evolutionary biology lingo, we would say that the common fruit fly underwent “positive selection” in its ADH gene, while the other fruit fly did not.

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Directed Evolution Wins Nobel Prize

From left to right: Dr. Frances Arnold, Sir Gregory Winter, Dr. George Smith
(Credits:Beavercheme2, Aga Machaj, Univ. Missouri-Columbia)

Yesterday, the Royal Swedish Academy of Sciences announced that the Nobel Prize in chemistry will be shared among three scientists who all used directed evolution to engineer proteins that solve problems. A reader who saw a news story about the announcement asked me to explain what “directed evolution” means, and I am happy to oblige. In directed evolution, scientists use the concepts of variation and selection to take a molecule that already exists in nature and adapt it to do something that they want it to do. Using a concrete example that comes from the research of Dr. Frances Arnold (one of the recipients) is probably the best way to explain the process.

Dr. Arnold’s lab started with a naturally-occurring enzyme charmingly named P450 BM3. Enzymes speed up specific chemical reactions, and P450 BM3 speeds up the reaction in which an oxygen atom is inserted between a carbon atom and a hydrogen atom in a fatty acid molecule. This is an important step in the process by which a living organism breaks down fatty acid molecules. Dr. Arnold’s lab was interested in doing the same kind of reaction, but on a different type of organic molecule: a small alkane. The enzyme P450 BM3 couldn’t initially do that. However, it could weakly speed up that reaction on large alkanes.

Since the enzyme could at least do that, Dr. Arnold thought that she could “tweak” it until it did exactly what she wanted it to do. However, enzymes are absurdly complicated molecules, and human science isn’t very good at making or understanding them. So she decided to let better organic chemists (bacteria) do the heavy lifting. Her lab took the gene that tells bacteria how to make P450 BM3 and subjected it to mutations. They then saw whether or not the resulting enzyme made by bacteria was any closer to being able to do what they wanted it to do. Maybe it did a better job speeding up the reaction on a large alkane, or maybe it was able to speed up the reaction on a shorter alkane. If that was the case, they saved that gene and allowed it to mutate more, seeing if any more progress could be made. If not, they threw it away and tried again.

This is why the process is called “directed evolution.” Dr. Arnold’s lab induced mutations (which are a source of genetic change in organisms) and then selected any enzyme that ended up being better at what they wanted it to do. With enough of those steps, they were able to get what they wanted: an enzyme that inserted an oxygen atom between a carbon atom and a hydrogen atom in a small alkane. In the end, the process had changed just over 2% of the molecule, but that was enough to change it from an enzyme that acted on fatty acids to one that acted on small alkanes.

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One Common Ediacaran Was Probably an Animal

A fossil similar to the one in which cholesterol remnants were found. (click for credit)

Several years ago, I wrote about the enigmatic fossils found in Ediacaran rock. Most scientists think such rocks are 635-540 million years old, and the fossils found in them have been the source of much controversy. Some paleontologists think they were “primitive” animals, some think they were lichens, some think they were fungi, some think they were giant protozoa, and some think that many of them aren’t even fossils. Well, based on some recent research, one Ediacaran fossil (Dickinsonia – an example is shown above) was most likely an animal.

The research was done by a team of scientists from Australia, Russia, and Germany. They collected Dickinsonia fossils from Ediacaran rock found on a cliff near the White Sea in Russia. This rock is thought to be 558 million years old. They found a thin layer of organic film on top of the fossils, and they chemically analyzed that film. They found cholestane, which is a chemical remnant of cholesterol. It is important to note that they didn’t find cholesterol itself. They found a decay product that indicates the one-time presence of cholesterol.

Why is this important? Cholesterol is a common component of animal cells, but significant amounts of it are not found in lichen, protozoa, or fungi. Thus, the one-time presence of cholesterol indicates that these fossils were animals. But couldn’t the cholestane be contamination? That’s a possibility, so the researchers chemically analyzed the rocks surrounding the fossils. In those rocks, they found little cholestane. Instead, they found the remnants of steroids that are commonly found in algae. So the cholestane is definitely associated with the fossils themselves and is probably not the result of contamination.

If a large number of the Ediacaran fossils end up being classified as animals, I think that will add to the long, long list of problems with flagellate-to-philosopher evolution. Since these fossils are supposed to have come before the better-known fossils found in the Cambrian, they would represent either the animal ancestors of the Cambrian organisms or some evolutionary offshoot that came from those animal ancestors. Either way, evolutionists are now faced with the task of trying to figure out some fairly close evolutionary relationship between the Ediacaran organisms and the Cambrian organisms. Given that these two sets of fossils are so radically different from one another, I suspect that will be a daunting task!

A Failed Test of Fossil Record Interpretation

When you read about earth history in most textbooks, lots of definitive statements are made concerning events that occurred in the distant past. For example, in Biology: How Life Works, Volume 1 (Morris et. al., Macmillan 2014, 2016), students are told:

A giant meteor struck Earth 66 million years ago, causing the extinction of dinosaurs and many other species…Researchers have documented other mass extinctions, but the event that eliminated the dinosaurs appears to be the only one associated with a meteorite impact. (p. 7)

Any unsuspecting student reading those words would think that we know that a mass extinction of dinosaurs occurred 66 million years ago, that it was definitely cause by a meteor impact, and that there have been other mass extinction events as well.

The problem, of course, is that definitive statements like the ones above come from interpretations of the fossil record. The fossil record itself is spotty at best, and the interpretations are based on all sorts of unverifiable assumptions. So the obvious question becomes, “How accurate are those interpretations?” That’s awfully hard to test, since we can’t go back in time and confirm them. However, the great thing about science is that original thinkers can come along and figure out ingenious ways to test what you might think is untestable.

A team of researchers from the Florida Museum of Natural History, the University of Bologna, the University of the Bahamas, and the State University of New York at Geneseo decided to test how well we know things like the mass extinction events discussed in the textbook I just quoted. They took a series of geological samples from the Po Plain in Italy that are supposed to represent what went on over the past 126,000 years. They specifically examined the mollusks in those samples, which leave behind hard shells.

Their test was both simple and brilliant: Imagine that a mass extinction event occurred right after the samples were taken, and all 119 identified species of mollusks that are currently living there had been wiped out. Would this hypothetical mass extinction be properly interpreted from the fossil remains in the geological samples that had been taken? Not surprisingly, the answer was a solid, “No!”

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This Could Be One of the Most Important Scientific Papers of the Decade

What best explains the common features shared by animals? According to this study, it’s the fact that they are designed.

More than eight years ago (have I really been blogging that long?), I was excited to see the appearance of a new peer-reviewed journal, BIO-Complexity. I thought it was going to have a lot of impact on the science of biology, but so far, its impact has been minimal. A few good studies (like this one and this one) have been published in it, but overall, it has not published the ground-breaking research I had hoped it would.

That might have changed. I just devoured the most recent study published in the journal, and I have to say, it is both innovative and impressive. It represents truly original thinking in the field of biology, and if further research confirms the results of the paper, we might very well be on the precipice of an important advancement in the field of biological taxonomy (the science of classifying living organisms).

The paper starts by detailing the fact that while evolutionists have always hoped that living organisms can be organized into a tree of life (starting with one universal common ancestor and branching into all known organisms), that hope has never been realized. In particular, when we look at organisms on the genetic level, no consistent tree can be produced. Instead, a “tree-like” arrangement can be made, but it needs all sorts of rescuing devices to explain the many inconsistencies that crop up.

Nevertheless, the fact that the structure somewhat resembles a tree tells us something. It tells us that the organisms we see today contain a lot of commonalities. However, since no consistent tree can be constructed, it is doubtful that those commonalities are the result of evolution. How, then, can scientists understand the “tree-like” structure of biological relationships?

The author of this new paper, Dr. Winston Ewert, makes a suggestion that is both innovative and, at the same time, so obvious it makes me wonder why I haven’t heard it before.

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No, We Won’t Have Dinosaurs in Two Years!

Even with a LOT of tinkering during embryonic development, only minor changes could be made in a chick’s skull.
(image from Bhullar et. al. article linked below)

A little while ago, I wrote an article about how silly “science journalism” can get. The article was about the popular media’s claim that scientists were about to bring mammoths back from extinction. I explained how the idea was based on real research, but the goal of the research was not to bring mammoths back from extinction. In addition, if anything concrete comes from the work, it will probably be decades from now. In response to that, a student sent me an even sillier article, which comes from that bastion of journalistic integrity, People. It states the following:

Famed paleontologist Dr. Jack Horner, who’s been a consultant on all four films and is the real-life inspiration for Jurassic Park’s dinosaur expert Dr. Alan Grant, believes we’re (optimistically) just five years away from genetically engineering a dinosaur.

This article was written back in 2015, so based on Dr. Horner’s optimistic projection, we should be just two years away from having dinosaurs roaming around in some laboratory.

So what is the source of Dr. Horner’s optimism? He thinks that birds evolved from dinosaurs, so he thinks that we could genetically “turn back the clock” and transform a bird into a dinosaur. He claims that this has already been done to some extent:

In what Horner calls a definitive “proof of concept,” a group at Harvard and Yale “just recently, within the last few weeks, were able to transform the head of a bird back to actually reverse-engineer the bird’s snout back into a dinosaur-like snout.”

There are so many things wrong with that statement, it is hard to know where to start. However, I will give it a try.

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“Nylon”-Digesting Bacteria are Almost Certainly Not a Modern Strain

This marine bacterium has the ability to digest nylon waste products, despite the fact that it doesn’t live in an environment that contains nylon waste products. (click for credit)

Evolutionists are fond of stating “facts” that aren’t anywhere near factual. For example, when I was at university, I was taught, as fact, that bacteria evolved the genes needed to resist antibiotics after modern antibiotics were made. As with most evolutionary “facts,” this turned out to be nothing more than wishful thinking on the part of evolutionists. We now know that the genes needed for antibiotic resistance existed in the Middle Ages and back when mammoths roamed the earth. They have even been found in bacteria that have never been exposed to animals, much less any human-made materials.

Of course, being shown to be dead wrong doesn’t produce any caution among evolutionists when it comes to proclaiming the “evidence” for evolution. When Dr. Richard Lenski’s Long Term Evolution Experiment (LTEE) produced bacteria that could digest a chemical called “citrate” in the presence of oxygen, it was hailed as definitive “proof” (a word no scientist should ever use) that unique genes can evolve as a result of random mutation and selection. Once again, that “fact” was demonstrated to be wrong in a series of experiments done by intelligent design advocates. They showed that this was actually the result of an adaptive mutation, which is probably a part of the bacterial genome’s design.

Recently, I learned about an impressive genetic study by young-earth creationists Sal Cordova and Dr. John Sanford. It lays waste to another evolutionary “fact” I was taught at university: the recent evolution of nylon-digesting bacteria. The story goes something like this: In 1975, Japanese researchers found some bacteria, which are now charmingly named Arthrobacteria KI72, living in a pond where the waste from a nylon-producing factory was dumped. The researchers found that this strain of bacteria could digest nylon. Well, nylon wasn’t invented until 1935, and there would be no reason whatsoever for a bacterium to be able to digest nylon before it was invented. Thus, in a mere 40 years, a new gene had evolved, allowing the bacteria to digest something they otherwise could not digest.

Of course, we now know that this story isn’t anywhere close to being true.

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Study of Mice Highlights the “Junk DNA” Myth

Junk DNA is a crucial to evolutionary theory, despite the fact that it most likely doesn’t exist to any significant extent.
The concept of “junk DNA” is crucial to evolutionary theory. For example, the “gold standard” of evolutionary simulations doesn’t produce any evolution unless at least 85% of the simulated DNA is junk. This is why so many evolutionists are fighting against the straightforward conclusions of the ENCODE series of studies, which indicate that at least 80% of the human genome is functional. Dr. Dan Graur, for example, has famously said that if ENCODE is right, then evolution is wrong.

As is the case with most evolution-inspired ideas, the more we learn about the natural world, the more it becomes obvious that there is very little “junk DNA” in nature. A recently-published study of gender in mice highlights this fact. In the study, an international collaboration of scientists examined the development of sexual characteristics in mice. As you probably already know, in mammals there is a pair of chromosomes referred to as sex chromosomes. If an individual has an X chromosome and a Y chromosome in that pair, he is a male. If the individual has two X chromosomes, she is a female.

But the development of the proper characteristics associated with each sex depends on what happens during embryonic development. For example, as a mammal embryo develops, it starts out producing ovaries. However, there is a gene on the Y chromosome called Sry. It produces a protein that controls the production of another protein, called SOX9. The SOX9 protein turns developing ovaries into testes. A male develops testes, then, because of the action of a gene on the Y chromosome. But as this latest study shows, there is more to it than that.

The scientists removed a small section of DNA from genetically-male mice. This section is found in what the authors refer to as a “gene desert,” a section of DNA that is devoid of genes. Nevertheless, when that small section of DNA was deleted, the genetically-male mice developed ovaries and female genitalia. Now please understand that the genes involved in the production and regulation of the SOX9 protein were not removed; only a small portion of what many would call “junk DNA” was removed. Nevertheless, without that section of DNA, the genetically-male mice did not produce enough SOX9 protein, so the ovaries continued to develop into ovaries, which then caused the production of female genitalia. As a result, the authors refer to this small section of DNA as a SOX9 “enhancer.” It enhances the production of SOX9 at just the right time, so the males develop the correct gender characteristics.

While the results of this study are fascinating, they are not surprising. After all, it has become more and more clear that the concept of “junk DNA” is a myth. As a result, it makes sense that even small sections of DNA have important functions, at least in certain stages of development or under certain conditions. The reason I am blogging about the study is because of something the lead author said in an article that was published on his institution’s website:

Our study also highlights the important role of what some still refer to as ‘junk’ DNA, which makes up 98% of our genome. If a single enhancer can have this impact on sex determination, other non-coding regions might have similarly drastic effects. For decades, researchers have looked for genes that cause disorders of sex development but we haven’t been able to find the genetic cause for over half of them. Our latest study suggests that many answers could lie in the non-coding regions, which we will now investigate further.

Indeed. As Dr. John Mattick so aptly put it more than a decade ago:

…the failure to recognise the implications of the non-coding DNA will go down as the biggest mistake in the history of molecular biology.