Satellite DNA: Critical Constituent of Chromosomes

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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).

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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.

Resources

Endnotes
  1. University of Michigan, “Scientists Discover a Role for ‘Junk’ DNA,” ScienceDaily (April 11, 2018), www.sciencedaily.com/releases/2018/04/180411131659.htm.
  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.

Discovery of Intron Function Interrupts Evolutionary Paradigm

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BY FAZALE RANA – MARCH 6, 2019

Nobody likes to be interrupted when they are talking. It feels disrespectful and can be frustrating. Interruptions derail the flow of a conversation.

The editors tell me that I need to interrupt this lead to provide a “tease” for what is to come. So, here goes: Interruptions happen in biochemical systems, too. Life scientists long thought that these interruptions disrupted the flow of biochemical information. But, it turns out these interruptions serve an important function, offering a rejoinder a common argument against intelligent design.

Now back to the lead.

Perhaps it is no surprise that some psychologists study interruptions1 with the hope of discovering answers to questions such as:

  • Why do people interrupt?
  • Who is most likely to interrupt?
  • Do we all perceive interruptions in the same way?

While there is still much to learn about the science of interruptions, psychologists have discovered that men interrupt more often than women. Ironically, men often view women who interrupt as ruder and less intelligent than men who interrupt during conversations.

Researchers have also found that a person’s cultural background influences the likelihood that he or she will interrupt during a discourse. Personality also plays a role. Some people are more sensitive to pauses in conversation and, therefore, find themselves interrupting more often than those who are less uncomfortable with periods of silence.

Psychologists have learned that not all interruptions are the same. Some people interrupt because they want the “floor.” These people are called intrusive interrupters. Cooperativeinterrupters help move the conversation along by agreeing with the speaker and finishing the speaker’s thoughts.

Interruptions are not confined to conversations. They are a part of life, including the biochemical operations that take place inside the cell.

In fact, biochemists have discovered that the information harbored in genes, which contains the instructions to build proteins—the workhorse molecules of the cell—experience interruptions in their coding sequences. These intrusive interruptions would disrupt the flow of information in the cell during the process of protein synthesis if the interrupting sequences weren’t removed by the cell’s machinery.

Molecular biologists have long viewed these genetic “interruptions” (called introns) as serving no useful purpose for the cell, with introns comprising a portion of the junk DNA found in the genomes of eukaryotic organisms. But it turns out that introns—like cooperative interruptions during a conversation—serve a useful purpose, according to the recent work of two independent teams of molecular biologists.

Introns Are Abundant

Noncoding regions within genes, introns consist of DNA sequences that interrupt the coding regions (called exons) of a gene. Introns are pervasive in genomes of eukaryotic organisms. For example, 90 percent of genes in mammals consists of introns, with an average of 8 per gene.

After the information stored in a gene is copied into messenger RNA, the intron sequences are excised, and the exons spliced together by a protein-RNA complex known as a spliceosome.

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Figure 1: Drawing of pre-mRNA to mRNA. Image credit: Wikipedia

Molecular biologists have long wondered why eukaryotic genes would be riddled with introns. Introns seemingly make the structure and expression of eukaryotic genes unnecessarily complicated. What possible purpose could introns serve? Researchers also thought that once the introns were spliced out of the messenger RNA sequences, they were discarded as genetic debris.

Introns Serve a Functional Purpose

But recent work by two independent research teams from Sherbrooke University in Quebec, Canada, and MIT, respectively, indicates that molecular biologists have been wrong about introns. They have learned that once spliced from messenger RNA, these fragments play a role in helping cells respond to stress.

Both research teams studied baker’s yeast. One advantage of using yeast as a model organism relates to the relatively small number of introns (295) in its genome.

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Figure 2: A depiction of baker’s yeast. Image credit: Shutterstock

Taking advantage of the limited number of introns in baker’s yeast, the team from Sherbrooke University created hundreds of yeast strains—each one missing just one of its introns. When grown under normal conditions with a ready supply of available nutrients, the strains missing a single intron grew normally—suggesting that introns aren’t of much importance. But when the researchers grew the yeast cells under conditions of food scarcity, the yeast with the deleted introns frequently died.2

The MIT team observed something similar. They noticed that during the stationary phase of growth (when nutrients become depleted, slowing down growth), introns spliced from RNA accumulated in the growth medium. The researchers deleted the specific introns that they found in the growth medium from the baker’s yeast genome and discovered that the resulting yeast strains struggled to survive under nutrient-poor conditions.3

At this point, it isn’t clear how introns help cells respond to stress caused by a lack of nutrients, but they have some clues. The Sherbrooke University team thinks that the spliced-out introns play a role in repressing the production of proteins that help form ribosomes. These biochemical machines manufacture proteins. Because protein synthesis requires building block materials and energy, during periods when nutrients are scarce, protein production slows down in cells. Ratcheting down protein synthesis impedes cell growth but affords them a better chance to survive a lack of nutrients. One way cells can achieve this objective is to stop making ribosomes.

The MIT team thinks that some spliced-out introns interact with spliceosomes, preventing them from splicing out other introns. When this disruption happens, it slows down protein synthesis.

Both research groups believe that in times when nutrients are abundant, the spliced-out introns are broken down by the cell’s machinery. But when nutrients are scarce, that condition triggers intron accumulation.

At this juncture, it isn’t clear if the two research teams have uncovered distinct mechanisms that work collaboratively to slow down protein production, or if they are observing facets of the same mechanism. Regardless, it is evident that introns display functional utility. It’s a surprising insight that has important ramifications for our understanding of the structure and function of genomes. This insight has potential biomedical utility and theological implications, as well.

Intron Function and the Case for Creation

Scientists who view biology through the lens of the evolutionary paradigm are 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 introns, 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, including introns, harbors function. In fact, many life scientists regard the “evolutionary vestiges” in the genome as junk DNA. This clearly has been the case for introns.

Yet, a growing body of data indicates that virtually every category of so-called junk DNA displays function. We can now add introns—cooperative interrupters—to the list. And based on the data on hand, we can make a strong case that most of the sequence elements in genomes possess functional utility.

Could it be that scientists really don’t understand the biology of genomes? Or maybe we have the wrong paradigm?

It seems to me that science is in the midst of a revolution in our understanding of genome structure and function. Instead of being a wasteland of evolutionary debris, most of the genome appears to be functional. And 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.

But what if the genome is viewed from a creation model framework?

The elegance and sophistication of genomes are features that are increasingly coming into scientific view. And this is precisely what I would expect if genomes were the product of a Mind—the handiwork of a Creator.

Now that is a discovery worth talking about.

Resources

Endnotes
  1. Teal Burrell, “The Science behind Interrupting: Gender, Nationality and Power, and the Roles They Play,” Post Magazine (March 14, 2018), https://www.scmp.com/magazines/post-magazine/long-reads/article/2137023/science-behind-interrupting-gender-nationality; Alex Shashkevich, “Why Do People Interrupt? It Depends on Whom You’re Talking To,” The Guardian (May 18, 2018), https://www.theguardian.com/lifeandstyle/2018/may/18/why-do-people-interrupt-it-depends-on-whom-youre-talking-to.
  2. Julie Parenteau et al., “Introns Are Mediators of Cell Response to Starvation,” Nature 565 (January 16, 2019): 612–17, doi:10.1038/s41586-018-0859-7.
  3. Jeffrey T. Morgan, Gerald R. Fink, and David P. Bartel, “Excised Linear Introns Regulate Growth in Yeast,” Nature 565 (January 16, 2019): 606–11, doi:10.1038/s41586-018-0828-1.

Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2019/03/06/discovery-of-intron-function-interrupts-evolutionary-paradigm

Protein-Binding Sites ENCODEd into the Design of the Human Genome

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BY FAZALE RANA – MARCH 15, 2017

At last year’s AMP Conference, I delivered a talk titled: “How the Greatest Challenges Can Become the Greatest Opportunities for the Gospel.” I illustrated this point by describing three scientific concepts related to the origin of humanity that 20 years ago stood as insurmountable challenges to the traditional biblical view of human origins. But, thanks to scientific advances, these concepts have been replaced with new insights that turn these challenges into evidence for the Christian faith.

The Challenge of Junk DNA

One of the challenges I discussed centered on junk DNA—nonfunctional DNA littering the genomes of most organisms. Presumably, these nonfunctional DNA sequences arose through random biochemical, chemical, and physical events, with functional DNA converted into useless junk, in some instances. In fact, when the scientific community declared the human genome sequence completed in 2003, estimates at that time indicated that around 95 percent of the human genome consist of junk sequences.

Since I have been involved in apologetics (around 20 years), skeptics (and believers) have regarded the high percentages of junk DNA in genomes as a significant problem for intelligent design and creation models. Why would an all-powerful, all-knowing, and all-good God create organisms with so much junk in their genomes? The shared junk DNA sequences found among the genomes of humans and the great apes compounds this challenge. For many, these shared sequences serve as compelling evidence for common ancestry among humans and the other primates. Why would a Creator introduce nonfunctional DNA sequences into corresponding locations in genomes of humans and the great apes?

But what if the junk DNA sequences are functional? It would undermine the case for common descent, because these shared sequences could reasonably be interpreted as evidence for common design.

The ENCODE Project

In recent years, numerous discoveries indicate that virtually every class of junk DNA displays function, providing mounting support for a common-design interpretation of junk DNA. (For a summary, see the expanded and updated edition of Who Was Adam?) Perhaps the most significant advance toward that end came in the fall of 2012 with the publication of phase II results of the ENCODE project—a program carried out by a consortium of scientists with the goal of identifying the functional DNA sequence elements in the human genome.

To the surprise of many, the ENCODE project reported that around 80 percent of the human genome displays function, with the expectation that this percentage should increase with phase III of the project. Many of the newly recognized functional elements play a central role in regulating gene expression. Others serve critical roles in establishing and maintaining the three-dimensional hierarchical structure of chromosomes.

If valid, the ENCODE results would force a radical revision of the way scientists view the human genome. Instead of a wasteland littered with junk DNA sequences, the human genome (and the genome of other organisms) would have to be viewed as replete with functional elements, pointing to a system far more complex and sophisticated than ever imagined—befitting a Creator’s handiwork. (See the articles listed in the Resources section below for more details.)

ENCODE Skeptics

Within hours of the publication of the phase II results, evolutionary biologists condemned the ENCODE project, citing a number of technical issues with the way the study was designed and the way the results were interpreted. (For a response to these complaints go herehere, and here.)

These technical complaints continue today, igniting the junk DNA war between evolutionary biologists and genomics scientists. Though the concerns expressed by evolutionary biologists are technical, some scientists have suggested the real motivation behind the criticisms of the ENCODE project are philosophical—even theological—in nature. For example, molecular biologists John Mattick and Marcel Dinger write:

There may also be another factor motivating the Graur et al. and related articles (van Bakel et al. 2010; Scanlan 2012), which is suggested by the sources and selection of quotations used at the beginning of the article, as well as in the use of the phrase ‘evolution-free gospel’ in its title (Graur et al. 2013): the argument of a largely non-functional genome is invoked by some evolutionary theorists in the debate against the proposition of intelligent design of life on earth, particularly with respect to the origin of humanity. In essence, the argument posits that the presence of non-protein-coding or so-called ‘junk DNA’ that comprises >90% of the human genome is evidence for the accumulation of evolutionary debris by blind Darwinian evolution, and argues against intelligent design, as an intelligent designer would presumably not fill the human genetic instruction set with meaningless information (Dawkins 1986; Collins2006). This argument is threatened in the face of growing functional indices of noncoding regions of the genome, with the latter reciprocally used in support of the notion of intelligent design and to challenge the conception that natural selection accounts for the existence of complex organisms (Behe 2003; Wells 2011).1

Is DNA-Binding Activity Functional?

Even though there may be nonscientific reasons for the complaints leveled against the ENCODE project, it is important to address the technical concerns. One relates to how biochemical function was determined by the ENCODE project. Critics argued that ENCODE scientists conflated biochemical activity with function. As a case in point, three of the assays employed by the ENCODE consortium measure binding of proteins to the genome, with the assumption that binding of transcription factors and histones to DNA indicated a functional role for the target sequences. On the other hand, ENCODE skeptics argue that most of the measured protein binding to the genome was random.

Most DNA-binding proteins recognize and bind to short stretches of DNA (4 to 10 base pairs in length) comprised of highly specific nucleotide sequences. But given the massive size of the human genome (3.2 billion genetic letters), nonfunctional binding sites will randomly occur throughout the genome, for statistical reasons alone. To illustrate: Many DNA-binding proteins target roughly between 1 and 100 sites in the genome. Yet, the genome potentially harbors between 1 million and 1 billion binding sites. The hundreds of sites that are slight variants of the target sequence will have a strong affinity to the DNA-binding proteins, with thousands more having weaker affinities. Hence, the ENCODE critics maintain that much of the protein binding measured by the ENCODE team was random and nonfunctional. To put it differently, much of the protein binding measured in the ENCODE assays merely is a consequence of random biochemical activity.

Nonfunctional Protein Binding to DNA Is Rare

This challenge does have some merit. But, this criticism may not be valid. In an earlier response to this challenge, I acknowledged that some protein binding in genomes will be random and nonfunctional. Yet, based on my intuition as a biochemist, I argued that random binding of proteins throughout the genome would be disruptive to DNA metabolism, and, from an evolutionary perspective would have been eliminated by natural selection. (From an intelligent design/creation model vantage point, it is reasonable to expect that a Creator would design genomes with minimal nonfunctional protein-binding sites.)

As it happens, new work by researchers from NYU affirms my assessment.2 These investigators demonstrated that protein binding in genomes is not random but highly specific. As a corollary, the human genome (and genomes of other organisms) contains very few nonfunctional protein-binding sites.

To reach this conclusion, these researchers looked for nonfunctional protein-binding sites in the genomes of 75 organisms, representative of nearly every major biological group, and assessed the strength of their interaction with DNA-binding proteins. The researchers began their project by measuring the binding affinity for a sample of regulatory proteins (from humans, mice, fruit flies, and yeast) with every possible 8 base pair sequence combination (32,896). Based on the binding affinity data, the NYU scientists discovered that nonfunctional binding sites with a high affinity for DNA binding proteins occurred infrequently in genomes. To use scientific jargon to describe their findings: The researchers discovered a negative correlation between protein-binding affinity and the frequency of nonfunctional binding sites in genomes. Using statistical methods, they demonstrated that this pattern holds for all 75 genomes in their study.

They attempted to account for the frequency of nonfunctional binding sequences in genomes by modeling the evolutionary process, assuming neutral evolution in which random mutations accrue over time free from the influence of natural selection. They discovered that this modeling failed to account for the sequence distributions they observed in the genomes, concluding that natural selection must have weeded high affinity nonfunctional binding sites in genomes.

These results make sense. The NYU scientists point out that protein mis-binding would be catastrophic for two reasons: (1) it would interfere with several key processes, such as transcription, gene regulation, replication, and DNA repair (the interference effect); and (2) it would create inefficiencies by rendering DNA-binding proteins unavailable to bind at functional sites (the titration effect). Though these problems may be insignificant for a given DNA-binding protein, the cumulative effects would be devastating because there are 100 to 1,000 DNA-binding proteins per genome with 10 to 10,000 copies of each protein.

The Human Genome Is ENCODEd for Design

Though the NYU researchers conducted their work from an evolutionary perspective, their results also make sense from an intelligent design/creation model vantage point. If genome sequences are truly the product of a Creator’s handiwork, then it is reasonable to think that the sequences comprising genomes would be optimized—in this case, to minimize protein mis-binding. Though evolutionary biologists maintain that natural selection shaped genomes for optimal protein binding, as a creationist, it is my contention that the genomes were shaped by an intelligent Agent—a Creator.

These results also have important implications for how we interpret the results of the ENCODE project. Given that the NYU researchers discovered that high affinity nonfunctional binding sites rarely occur in genomes (and provided a rationale for why that is the case), it is difficult for critics of the ENCODE project to argue that transcription factor and histone binding assays were measuring mostly random binding. Considering this recent work, it makes most sense to interpret the protein-binding activity in the human genome as functionally significant, bolstering the original conclusion of the ENCODE project—namely, that most of the human genome consists of functional DNA sequence elements. It goes without saying: If the original conclusion of the ENCODE project stands, the best evidence for the evolutionary paradigm unravels.

Our understanding of genomes is in its infancy. Forced by their commitment to the evolutionary paradigm, many biologists see genomes as the cobbled-together product of an unguided evolutionary history. But as this recent study attests, the more we learn about the structure and function of genomes, the more elegant and sophisticated they appear to be. And the more reasons we have to believe that genomes are the handiwork of our Creator.

Resources

Endnotes

  1. John S. Mattick and Marcel E. Dinger, “The Extent of Functionality in the Human Genome,” The HUGO Journal 7 (July 2013): doi:10.1186/1877-6566-7-2.
  2. Long Qian and Edo Kussell, “Genome-Wide Motif Statistics Are Shaped by DNA Binding Proteins over Evolutionary Time Scales,” Physical Review X 6 (October–December 2016): id. 041009, doi:10.1103/PhysRevX.6.041009.
Reprinted with permission by the author
Original article at:
https://www.reasons.org/explore/blogs/the-cells-design/read/the-cells-design/2017/03/15/protein-binding-sites-encoded-into-the-design-of-the-human-genome