March 2, 2020 | Jerry Bergman

Jumping Genes: From Genome Havoc to Designed Variety


Another New Discovery of their Function

by Jerry Bergman, PhD

Each step taken in analyzing the human genome reveals not only more complexity, but also more evidence of design. As is often said, genetics has not turned out to be a friend of evolution. As time goes on, this claim has become more meaningful. A major discovery was made by Barbara McClintock in 1951. Gleaned from her research on maize corn, she discovered controlling (transposable) elements called ”jumping genes” (e.g., plasmids and transposons). These are sections of DNA that can literally cut themselves out of their original location and move elsewhere in the genome. They can then splice themselves into their new home.1

Intolerance for a Paradigm Shift

It was a controversial finding that appeared far too unrealistic for the genetics community, and they told her so in no uncertain terms. The thought of a gene cutting itself out of one location and then moving somewhere else, then splicing itself into the new location, sounded almost as if the gene has a conscious mind to make travel decisions. The response to her findings was, in McClintock’s words,

in some instances, hostility. A third attempt to support the thesis of the origin of mutable loci in maize appeared in 1953 in the widely read journal Genetics. It was titled “The Induction of Instability at Selected Loci in Maize.”… I received a total of only three requests for this reprint! By then I had already concluded that no amount of published evidence would be effective… There were many vocal skeptics. Therefore, the method I had chosen to record data and conclusions from them was continued into the early 1960s…. In retrospect, it appears that the difficulties in presenting the evidence and arguments for transposable elements in eukaryotic organisms were attributable to conflicts with accepted genetic concepts. That genetic elements could move to new locations in the genome had no precedent and no place in these concepts.2

Based on the very negative reactions of other scientists to her work, from 1953 forward, McClintock was forced to stop publishing accounts of her research. At the time, geneticists accepted the “central dogma” of genetics: namely, that DNA was the “master molecule” that acted as a static library read by other machines. In time, though, other researchers and discoveries supported her work. Many years later, she was vindicated. She was eventually awarded the Nobel Prize for her research on these unexpected transposons.3

The phenomenon of “jumping genes” has now been determined to be far more complex than even McClintock postulated. It has also been shown to be more common than anyone predicted. Transposable elements are now believed to make up fully half of the mammalian genome, indicating that they must be strictly regulated – otherwise they would cause havoc in the genome in only a few short generations. The question of why transposable elements do not wreak havoc, and have not done so, has stymied evolutionary geneticists.4 Creationist geneticists are not surprised. They believe that the entire transposition system is designed to reach specific goals, including designed diversity.

McClintock’s Research

Maize corn kernels have what was then judged as unstable phenotypes in kernel color, and McClintock wanted to find out why. She fathomed that an unstable phenotype was not the reason. Instead, she contemplated that because all of the kernels were produced by the same gene, something must have been turning the pigment gene on or off, or in some way affecting the interplay between a transposable element (TE) and a pigment gene.

In short, her concern was the means of regulating the suppression and expression of genetic information from one generation of maize plants to the next. She called the units that regulated the expression controlling elements to distinguish them from genes. Eventually, she discovered the controlling elements moved around, a finding that led to postulate the transposon theory. From her research, McClintock was also the first scientist to speculate on the concept of epigenetics, i.e., heritable changes in gene expression that are not caused by changes in DNA sequences.

It was once thought, based on evolutionary assumptions, that transposable elements primarily moved randomly from one spot in the genome to another location. With more research it was discovered that the locations where they spliced themselves in were most often not random, but to positions now called hot spots.5 This view, which supported the design theory, has now been confirmed by empirical research.

DNA coils and supercoils in a highly regulated way to pack the genome into chromosomes so that they can fit in the cell nucleus.

New Research Finds Yet Another Role for Transposons

Scientists at Washington University School of Medicine in St. Louis have just announced yet another role for jumping genes: they help to stabilize DNA folding patterns.6 DNA folding in the nucleus is a big challenge for a cell. All of the DNA inside the nucleus of every human cell is over six feet long, or 1,828,800 µm (micrometers), but the average diameter of the nucleus—the largest organelle in animal cells, occupying about ten percent of the total cell volume in mammalian cells—is approximately 6 µm long. Thus, the DNA is close to 304,800 times longer than the average mammalian cell nucleus! Consequently, to fit this 1,828,800 µm total length molecule into the nucleus, it must fold into thousands of precise loops called supercoils. The specific folding pattern must also be tightly controlled because the organization of the folds regulates gene expression.

New research has found evidence that ‘jumping genes’ play a major role in stabilizing DNA’s 3D folding pattern that enables it to fit inside of the cell’s nucleus. Fitting the six feet of DNA into the close-to-submicroscopic nucleus is an amazing feat. The researchers found:

In places where the larger 3D folding of the genome is the same between mice and humans, you expect the sequence of the letters of the DNA anchoring that shape to be conserved there as well. But that’s not what we found, at least not in the portions of the genome that in the past have been called ‘junk DNA.’ … in many regions where the folding patterns of DNA are conserved through evolution, the genetic sequence of the DNA letters establishing these folds is not. It is ever so slightly displaced.7

Furthermore, the fact that a

transposable element can insert itself and serve the same role as an existing anchor creates a redundancy in the regulatory portions of the genome – regions of the DNA molecule that determine how and when genes are turned on or off…. this redundancy makes the genome more resilient. In providing both novelty and stability, jumping genes may help the mammalian genome strike a vital balance – allowing animals the flexibility to adapt … while preserving biological functions required for life.8

Surveys of genomes from a large number of people have identified much variation in non-coding regions that do not appear to have any effect on gene regulation, a very puzzling problem. The new understanding of transposable elements appears to explain this problem: the local sequence can vary, but the folding role remains the same: the DNA still folds in the same location. This finding leads the researchers to believe that transposons in the non-protein-coding regions in the genome follow different rules than the protein-coding regions. Although

genome folding is largely conserved in mammals, the genetic forces shaping its emergence and evolution remain poorly understood. Two distinct yet mutually non-exclusive models have recently gained much traction: that of phase separation and of loop extrusion.9

How this dual function of transposons operates can only, at best, be postulated at this point. The research reviewed here has provided the data that now must be understood in terms of physical events which will, no doubt, challenge the best minds in the field. Once the specific mechanism is determined, the finding will certainly increase the complexity of the transposition system and provide even more evidence of design than the original discovery of the transposition mechanism, which is still not fully understood in spite of the fact that leading Harvard geneticists and others have been working on trying to understand it for almost 70 years.


Rather than a printed book, the genome may be more accurately likened to a manuscript stored on a word processing program. The information in the manuscript is not set in stone but is changeable or modifiable in ways that biologists are just beginning to understand. Evolutionary naturalism postulates the genome accumulated as a result of the selection of random mutations that have occurred throughout evolutionary history. Research in the genome, such as transposition, indicates that a far greater level of complexity exists in the genome than previously imagined. This complexity is certainly not due to random mutations which would soon wreak havoc to the genome.11


1 McClintock, Barbara. 1951. Chromosome organization and genic expression. Cold Spring Harbor Symposia on Quantitative Biology 16:13-47.
2 McClintock, Barbara. 1987. The Discovery & Characterization of Transposable Elements: The Collected Papers (1938-1984) of Barbara McClintock. New York, NY: Routledge Publishing.
McClintock, 1987.
Choudhary, M., et al. 2020. Co-opted transposons help perpetuate conserved higher-order chromosomal structures. Genome Biology 21:16 & 28, January 24 & February 7. p. 1.
Craig, Nancy L. 1997. Target site selection in transposition. Annual Review of Biochemistry 66:437-474.
6 Strait, Julia Evangelou. 2020. ‘Jumping genes’ help stabilize DNA folding patterns: Long understood as source of novel genetic traits, jumping genes also provide genomic stability. Washington University School of Medicine in St. Louis.,
7 Strait, 2020.
8 Strait, 2020.
9 Choudhary, et al., 2020.
10 Hadler, H.I.; Devadas, K.; and Mahalingam, R. 1998. Selected nuclear Line elements with mitochondrial-DNA-like inserts are more plentiful and mobile in tumor than in normal tissue of mouse and rat. Journal of Cellular Biochemistry 68(1):100-109, January 1.
11 Bergman, Jerry. 2001. “The Molecular Biology of Genetic Transposition.” CRSQ 38(3):139-150, December.

Dr. Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology for over 40 years at several colleges and universities including Bowling Green State University, Medical College of Ohio where he was a research associate in experimental pathology, and The University of Toledo. He is a graduate of the Medical College of Ohio, Wayne State University in Detroit, the University of Toledo, and Bowling Green State University. He has over 1,300 publications in 12 languages and 40 books and monographs. His books and textbooks that include chapters that he authored are in over 1,500 college libraries in 27 countries. So far over 80,000 copies of the 40 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.







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