email - May 2018
by Do-While Jones

A Maize-ing Science

Barbara McClintock’s study of the genetics of maize doesn’t support evolution.

We are grateful to Greg for sending us this email:

Hello Mr. Pogge,

I recently listened to a podcast where the host interviewed Perry Marshall, author of the book Evolution 2.0. He wrote his book after seeking to find the “the truth” about Evolution. He said that in his research, he read about epigenetics, which he claims is one of the mechanisms by which evolution works, and how we all evolved from a common ancestor.

He also mentioned the work of a woman named Barbara McClintock, who back in 1944, used radiation to damage the DNA of some corn and observed the plant repair its DNA by creating new code to fill in the holes left by the damage.  This, he claimed, is evidence that organisms can and do create new, functional genetic code.

I'm a little confused about how Marshall could think that epigenetic changes could result in any kind of long-term evolutionary process.  In my reading on the subject, my understanding was that although phenotypic epigenetic changes may be passed on, the genotype is never changed (and wouldn't even the phenotypic changes be limited?).

As far as McClintock’s research is concerned, this is something I was not aware of before. My first inclination was to think that if the plant repaired its DNA by “making do” with what it had left, wouldn’t the repair job be of lower quality than the original? For instance, I’m sure if a couple of the legs on one of my kitchen chairs broke, I could use what wood and tools I have on hand to functionally repair them (many could no doubt do better than I), but they would most likely be inferior to the original, not as good or better. Of course, I could be wrong in my assessment of McClintock’s work.

Since you’ve touched on epigenetics already in the past, I’m interested in your thoughts on Marshall’s book in general (if you’re familiar with it) and McClintock’s research as it relates to organisms creating new, functional genetic code as a possible evolutionary mechanism.


I am a little bit embarrassed to admit that I, too, was not familiar with Barbara McClintock’s research before getting Greg’s email. Now that I have read it, I am a big fan of her work.

It is easy to find biographical information about her in the professional literature. In a review of a book about her life, the reviewer wrote:

McClintock's life spanned that history [of modern genetics]. She was born in 1902, two years after the rediscovery of Mendel's laws by Correns and de Vries. She died in 1992, two years after the start of the Human Genome Project. As a working scientist at Cold Spring Harbor Laboratory for the last fifty years of her life, McClintock was at the best possible location to influence and be influenced by the leaders in the field. As the world's premier cytologist and the discoverer of transposable elements, it is inconceivable that she would not be an active participant in this history. 1

This review encouraged me to read her research. I found the paper she delivered in Stockholm, Sweden, 8 December 1983, when she received the Nobel Prize in Physiology or Medicine. In it, she described the research she did in 1944. It was unlike anything you read in the scientific journals today because it was full of real science! She made observations, did experiments, described what she did, and reported the results without contaminating them with unwarranted speculation. It was just so refreshing to read pure science!

She began her paper with this observation:

There are "shocks" that a genome must face repeatedly, and for which it is prepared to respond in a programmed manner. Examples are the "heat shock" responses in eukaryotic organisms and the "SOS" responses in bacteria. Each of these initiates a highly programmed sequence of events within the cell that serves to cushion the effects of the shock. Some sensing mechanism must be present in these instances to alert the cell to imminent danger, and to set in motion the orderly sequence of events that will mitigate this danger. But there are also responses of genomes to unanticipated challenges that are not so precisely programmed. The genome is unprepared for these shocks. Nevertheless, they are sensed, and the genome responds in a discernible but initially unforeseen manner. 2

If you cut your finger, your body responds by clotting the blood where the wound occurred. That is a programmed response to a shock. Dr. McClintock says, just like an entire organism responds to a shock, the same thing happens at the cellular level. Unless you are a cell biologist, you’ve never seen that happen—but she has. Other biologists have, too. They know that if a cell gets too hot (or too cold) the cell responds in a programmed manner to cushion the effects of the harmful temperature. She didn’t say this is evidence of design or evidence of evolution. She merely stated that it happens, and has been observed to happen, and is well documented. She was a good scientist.

Neither creationists nor evolutionists are surprised that genomes respond to normal shocks. Creationists aren’t surprised because they think the cell was designed to handle shocks. Evolutionists aren’t surprised because they think the response evolved through natural selection.

What was surprising to her was that genomes apparently have a defense mechanism against unforeseen shocks. For example, one can shock a cell by zapping it with radiation strong enough to damage the DNA. It certainly might surprise an evolutionist that cells have evolved a defense mechanism against a previously unexperienced challenge. Even a creationist might be surprised that cells were designed to repair their DNA after being exposed to an unnatural amount of radiation.

Dr. McClintock didn’t try to prove that these responses prove evolution or creation. She was smart enough to know that there is no scientific way to prove whether this remarkable biological mechanism accidentally evolved or was intentionally created. She just wanted to find out how it worked.

It is the purpose of this discussion to consider some observations from my early studies that revealed programmed responses to threats that are initiated within the genome itself, as well as others similarly initiated,- that lead to new and irreversible genomic modifications. 3

She did this by damaging the DNA of maize (corn) and examined the DNA of succeeding generations to see how it repaired itself.

Experiment with Zea mays in the Summer of 1944 and Its Consequences

The experiment that alerted me to the mobility of specific components of genomes involved the entrance of a newly ruptured end of a chromosome into a telophase nucleus. This experiment commenced with the growing of approximately 450 plants in the summer of 1944, each of which had started its development with a zygote that had received from each parent a chromosome with a newly ruptured end of one of its arms. … Each mutant was expected to reveal the phenotype produced by a minute homozygous deficiency and to segregate in a manner resembling that of a recessive in an F2 progeny. Their modes of origin could be projected from the known behavior of broken ends of chromosomes in successive mitoses. 4

(If you aren’t familiar with the genetic jargon, you can think of the genotype as a genetic blueprint and the phenotype as structure built from that blueprint. If you make a change to the blueprint, it changes how the building is built, and the change will probably be visible.)

She expected that the part of the gene that was damaged would result in a particular deformity in the maize containing that damaged gene. She expected to be able to segregate (to sort) the resulting plants into differently damaged categories depending upon what part of the gene was damaged. And she could—sometimes.

Some seedling mutants of the type expected did segregate, but they were overshadowed by totally unexpected segregants exhibiting bizarre phenotypes. 5

To put it simply, some of the leaves and ears of corn were strangely (bizarrely) colored and misshapen in totally unexpected ways. She wanted to know why.

After observing many such twin sectors, I concluded that regulation of pattern of gene expression in these instances was associated with an event occurring at a mitosis in which one daughter cell had gained something that the other daughter cell had lost. Believing that I was viewing a basic genetic phenomenon, all attention was given, thereafter, to determining just what it was that one cell had gained that the other cell had lost. These proved to be transposable elements that could regulate gene expressions in precise ways. Because of this I called them "controlling elements." Their origins and their actions were a focus of my research for many years thereafter. 6

She found that an undamaged part of the DNA from a different location on the DNA molecule could transpose (move) and splice itself into the damaged section. This changed the genotype, which manifested itself in a physically observable change to the phenotype.

A conclusion of basic significance could be drawn from these observations: broken ends of chromosomes will fuse, two-by-two, and any broken end with any other broken end. This principle has been amply proved in a series of experiments conducted over the years. In all such instances the break must sever both strands of the DNA double helix. This is a "double-strand break" in modem terminology. That two such broken ends entering a telophase nucleus will find each other and fuse, regardless of the initial distance that separates them, soon became apparent. …

The conclusion seems inescapable that cells are able to sense the presence in their nuclei of ruptured ends of chromosomes and then to activate a mechanism that will bring together and then unite these ends, one with another. And this will occur, regardless of the initial distance in a telophase nucleus that separated the ruptured ends. The ability of a cell to sense these broken ends, to direct them toward each other, and then to unite them so that the union of the two DNA strands is correctly oriented, is a particularly revealing example of the sensitivity of cells to all that is going on within them. 7

All of this is real science. It started with an observation. Possible mechanisms were proposed. Experiments were done to confirm or deny the proposed mechanisms. A shocking, inescapable conclusion was reached. “Cells are able to sense the presence in their nuclei of ruptured ends of chromosomes and then to activate a mechanism that will bring together and then unite these ends.”

Cells appear to be a lot like computers in this respect. Computers can be programmed to respond to inputs from their sensors. For example, a computer could use a moisture detector to decide when to turn on the sprinklers and water the crops. But someone has to be smart enough to know how to program it to do the proper thing.

More Questions

As is often the case, when studying a phenomenon carefully, observations are made which raise more questions.

A goal for the future would be to determine the extent of knowledge the cell has of itself and how it utilizes this knowledge in a "thoughtful" manner when challenged. 4

That sentence probably makes evolutionists uncomfortable. It is awfully hard to believe that a single cell is self-aware, and has the intelligence to adapt to its surrounding, simply because of Darwinian Evolution.

The notion of programmed responses raises the question of Intelligent Design, which must not be acknowledged in modern, polite, biological company. Fortunately, Dr. McClintock was able to present the truth honestly in 1984 because that was about five years before the concept of Intelligent Design was proposed and became prohibited speech.

A Galling Observation

The second related question for evolutionists is galling (in both senses of the word).

One class of programmed responses to stress has received very little attention by biologists. Here a stress signal induces the cells of a plant to make a wholly new plant structure, and this to house and feed a developing insect, from egg to the emerging adult. A single Vitis plant, for example, may have on its leaves three or more distinctly different galls, each housing a different insect species. The stimulus associated with placement of the insect egg into the leaf will initiate reprogramming of the plant's genome, forcing it to make a unique structure adapted to the needs of the developing insect. The precise structural organization of a gall that gives it individuality must start with an initial stimulus, and each species provides its own specific stimulus. For each insect species the same distinctive reprogramming of the plant genome is seen to occur year after year. Some of the most interesting and elaborate plant galls house developing wasps. Each wasp species selects its own responding oak species, and the gall structure that is produced is special for each wasp to oak combination. All of these galls are precisely structured, externally and internally, as a rapid examination of them will show. 8

This is related to her original research about how genomes respond to shocks. An insect shocks a plant, and the plant responds by producing a gall (a wart, for lack of a better description) which houses and nourishes the insect. How do the insects know which plants to shock to make them produce a specialized gall that will provide them the necessary functionality? Why do the plants want to be so hospitable? It really suggests some sort of coordinator directing the insects and preprogramming the plants.

Here is how she concluded her paper accepting the Nobel Prize:

Concluding Statement

The purpose of this discussion has been to outline several simple experiments conducted in my laboratory that revealed how a genome may react to conditions for which it is unprepared, but to which it responds in a totally unexpected manner. Among these is the extraordinary response of the maize genome to entrance of a single ruptured end of a chromosome into a telophase nucleus. It was this event that, basically, was responsible for activations of potentially transposable' elements that are carried in a silent state in the maize genome. The mobility of these activated elements allows them to enter different gene loci and to take over control of action of the gene wherever one may enter.

In the future, attention undoubtedly will be centered on the genome, with greater appreciation of its significance as a highly sensitive organ of the cell that monitors genomic activities and corrects common errors, senses unusual and unexpected events, and responds to them, often by restructuring the genome. We know about the components of genomes that could be made available for such restructuring. We know nothing, however, about how the cell senses danger and instigates responses to it that often are truly remarkable. 9

The notion that a single cell can sense danger and respond appropriately to that danger really is, as she says, “extraordinary” and “remarkable.” Evolutionists just chalk it up to good luck, filtered by natural selection.

Her prediction about the importance of genomic studies is so obvious to us today that it hardly seems worth mentioning. But, in 1984, she was one of only a few individuals to recognize its importance.

Greg’s Question

All of this background was necessary to answer Greg’s question about “McClintock’s research as it relates to organisms creating new, functional genetic code as a possible evolutionary mechanism.”

McClintock’s research showed that when DNA is damaged, other DNA fragments can be grafted into that spot on the genome, which changes the resulting phenotype. (As we said before, changing the blueprint changes the building.) The technical term is “transposition.” Pieces of DNA are transposed (moved) from one place to another. Her research proved that really happens, and she got the Nobel Prize for it.

Evolutionists believe that gene duplication and transposition create information, which is how (for example) reptiles grew mammary glands and became mammals. As crazy as that sounds, some evolutionists really believe it.

In particular, Jeff wrote to us in September, 2005, to say that duplication of genes increases information. In our response, 10 we tried to show that repeating random parts of his email did not increase its information content. Argumentative Alex responded with an email to us in October, 2005, trying to defend Jeff. 11 We encourage you to go back to read our responses to those two previous emails.

Dr. McClintock’s paper also mentioned the fact that hybridization can produce new characteristics. Anyone who has ever lived in Nebraska can testify to the existence of many different brands of hybrid corn, as evidenced by the roadside signs at the edge of cornfields. Genetic information from other species can be bred into the genome to produce (or enhance) certain characteristics.

Regardless of whether the new genetic information came from a different species, or a different place on the individual’s own genome, one fact remains: the information was already there—it wasn’t created out of thin air.

Transposition of genetic elements from one place to another does explain how changes to the genotype cause changes in the phenotype—but it doesn’t explain the origin of those genetic elements. That’s the problem evolutionists can’t solve.

Debate Class

Imagine you are in a high school debate class. The proposition is: “Dr. McClintock’s research is more consistent with Intelligent Design than Darwinian Evolution.” Everyone on the winning side will get an A. Everyone on the losing side fails the class. You can choose to take either side. Which side would you choose to be on?

Quick links to
Science Against Evolution
Home Page
Back issues of
(our newsletter)
Web Site
of the Month
Topical Index


1 Susan R. Wessler, Science, 5 Oct 2001, “McClintock at 100--Reason to Celebrate”,
2 Barbara McClintock, Science, 16 November 1984, “The Significance of Responses of the Genome to Challenge”, page 792,
3 ibid. pp. 792-793
4 ibid. p. 793
5 ibid. p. 793
6 ibid. p. 793
7 ibid. p. 794
8 ibid. p. 798
9 ibid. p. 798
10 ibid. pp. 800-801
11 Disclosure, September 2005, “Gene Duplication”
12 Disclosure, October 2005, “Gene Duplicatioioion”, “Gene Duplicatioioion”