'Junk DNA' Genomics Intelligent Design Neuroscience

New use for “junk DNA”: Controlling fear

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As the genome responds to traumatic experiences:

A piece of “junk DNA” could be the key to extinguishing fear-related memories for people struggling with post-traumatic stress disorder (PTSD) and phobia, according to a study from The University of Queensland.

An international research project, led by the Queensland Brain Institute’s Associate Professor Timothy Bredy, discovered the new gene while investigating how the genome responds to traumatic experiences.

“Until recently, scientists thought the majority of our genes were made up of junk DNA, which essentially didn’t do anything.” Dr. Bredy said.

“But when researchers began to explore these regions, they realized that most of the genome is active and transcribed.”

University of Queensland, “‘Junk DNA’ could be key to controlling fear” at Phys.org (March 22, 2022)

Okay, why, until recently, did researchers think that “the majority of our genes were made up of junk DNA, which essentially didn’t do anything”?

Because that vast sunken library of dead information (sheer randomness and waste) was a slam dunk for Darwinism, as politically powerful theistic evolutionist Francis Collins was quick to point out in The Language of God. (2007). To say nothing of atheist cultural icon Richard Dawkins here, Darwinian evolutionary biologist Jerry Coyne (here), and unidirectional skeptic Michael Shermer (here). Notice how that history is quietly being erased. Otherwise, it would be necessary to acknowledge that what many regarded as a correct prediction from Darwinism is not true.

So now what about fear?

“Our findings suggest that long non-coding RNAs provide a bridge, linking dynamic environmental signals with the mechanisms that control the way our brains respond to fear,” Dr. Bredy said.

“With this new understanding of gene activity, we can now work towards developing tools to selectively target long non-coding RNAs in the brain that directly modify memory, and hopefully, develop a new therapy for PTSD and phobia.”

University of Queensland, “‘Junk DNA’ could be key to controlling fear” at Phys.org (March 22, 2022)

Here’s the proposed mechanism:

'Junk DNA' key to controlling fear
Graphical abstract. Credit: Cell Reports (2022). DOI: 10.1016/j.celrep.2022.110546

Certainly worth pursuing in terms of addressing PTSD and phobias, as the authors note.

The paper is open access.

You may also wish to read: A new, useful, description for (former) junk DNA… ? “the large proportion of our genome that does not instruct our cells to form proteins” The phrase is a bit longish, of course, but concision is usually a product of usage. It’s better than “non-coding DNA” because it’s more specific and limited as a privative. That is, there is a specific thing that that vast mass of DNA does not do. The longish phrase does not come with the implication that it doesn’t do anything.

19 Replies to “New use for “junk DNA”: Controlling fear

  1. 1
    jerry says:

    DNA has nothing to do with Evolution.

    Junk DNA exists. Because 100% of it is not functional (some is functional) does not mean some is not functional. (all is not functional)

    And because some is not functional does not mean that it is not the result of some designed process that is functional.

    People are obsessed with proving a valid process invalid, namely Darwinian change which is 100% valid and scientific. The sooner this is admitted, the sooner the truth will emerge.

    Is ID doing a major disservice to the science community just as conventional science is doing a major disservice by exaggerating what a valid but limited process can do?

    Question: Are both sides not interested in the truth?

  2. 2

    You know that you are at stage #4 in the acceptance of a theory? Congratulations!
    1) Utter nonsense, give it no oxygen
    2) Dangerous nonsense must be stopped
    3) Partly true, but fatally flawed
    4) Trivially true, but emphasis wrong
    5) We knew it all along

  3. 3
    polistra says:

    “Old wives tales” told us that memories of scary and traumatic experiences were transferred from mother to child. Turns out they were exactly on target.

  4. 4
    jerry says:

    You know that you are at stage #4 in the acceptance of a theory? Congratulations!

    Been there done that over 15 years ago on this site.

    Is the problem few others are? Nothing has changed here. Most on both sides seem to be at 2.

    Actually, I personally believe I’m at 5, have been for years. But certainly not “we.” Is it possible to be personally at 5 or that is only a group phenomenon?

    Also is it arrogant and presumptuous to ever claim to be at 5? Happy to be at 4.



    Should the objective of UD be to get most of world to 5. They may claim that but the world is not moving there. So is UD failing?

  5. 5
    Silver Asiatic says:

    In 2009, University of Chicago geneticist Jerry A. Coyne compared predictions based on intelligent design with those based on Darwinian evolution. “If organisms were built from scratch by a designer,” he argued, they would not have imperfections.

    That’s gold.

  6. 6
    DATCG says:

    How do you define “Darwinian Change? Does this include macro-evolution using JUNK DNA?
    Or what current version of “Darwinism”? Seems neo-Darwinism is on the cutting board.

    As for JUNK DNA. For decades Darwinist blindly mislead people that over 90% of DNA was JUNK.
    This is all I heard in college by our professors, 98% until recent years. I’m not aware of ID leaders and scientist stating “all” JUNK DNA has function. Maybe there are some?
    Articles I read at sites like Evolution News do acknowledge JUNK DNA exist.
    They’re usually careful to say how much is functional is still an open question.

    How much JUNK DNA is required for neo-Darwinism to create macro changes over time?
    Is there a limit thresh hold for least amount of JUNK? An amount of JUNK DNA that must be accessible for use by random, blind forces? Maybe someone has advanced this in detail?

  7. 7
    jerry says:

    How do you define “Darwinian Change

    1) variation in genome – well established
    2)inheritance of this variation – well established
    3) natural selection affects genome – well established

    100% established in genetics. So valid science.

    No evidence this has any role in Evolution.

    Articles I read at sites like Evolution News do acknowledge JUNK DNA exist.

    Just what I said above. Some has function but has no relevance for Evolution.

    I use Evolution with a capital “E” to distinguish it from any change in genome over time.

  8. 8
    bornagain77 says:

    How do you define “Darwinian Change” (?)

    “1) variation in genome – well established”

    You forgot to mention that Darwinists hold, as a primary presupposition, that it is not directed variation in the genome, but that it is ‘random’ variation in the genome. That is NOT a minor omission.

    Revisiting the Central Dogma in the 21st Century – James A. Shapiro – 2009
    Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, (Page 14) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112).

    “It is difficult (if not impossible) to find a genome change operator that is truly random in its action within the DNA of the cell where it works. All careful studies of mutagenesis find statistically significant non-random patterns”
    James Shapiro – Evolution: A View From The 21st Century – (Page 82)

    Genome Self-Editing – directed mutations – (JohnnyB) video (2021)

    “2) inheritance of this variation – well established”

    You forgot to mention that most, if not all, of the inherited variation is found to be a result of loss of genetic information, not gain of genetic information. (Which is, again, contrary to a primary presupposition within Darwinian evolution). See Behe; “Darwin Devolves” and Sanford; “Genetic Entropy”

    “3) natural selection affects genome – well established”

    Well actually, save for minor examples of antibiotic resistance etc., there is very little empirical evidence for natural selection doing much of anything within the genome.

    Genome-wide analysis of a long-term evolution experiment with Drosophila – 2010
    Excerpt of concluding paragraph: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles. This is notable because in wild populations we expect the strength of natural selection to be less intense and the environment unlikely to remain constant for ~600 generations. Consequently, the probability of fixation in wild populations should be even lower than its likelihood in these experiments.”

    “The Third Way” – James Shapiro, Denis Noble, and etc.. etc..,,,
    Excerpt: “some Neo-Darwinists have elevated Natural Selection into a unique creative force that solves all the difficult evolutionary problems without a real empirical basis.”

    “the uncritical acceptance of natural selection as an explanatory force for all aspects of biodiversity (without any direct evidence) is not much different than invoking an intelligent designer”
    Michael Lynch – The Origins of Genome Architecture, p 368

    Moreover, besides empirical evidence not supporting your claim that natural selection is ‘well established’, natural selection is also certainly not ‘well established’ within the mathematics of population genetics,

    The waiting time problem in a model hominin population – 2015 Sep 17
    John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner
    Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,,
    Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information.
    While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man.
    It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years.


    1 Thessalonians 5:21
    but test all things. Hold fast to the good.

  9. 9
    DATCG says:

    Thanks, been long time since I read or posted here so do not remember your position on this.
    So Evolution w/ capital E is Macro-Evolution? And to be clear, you’re stating JUNK DNA has nothing to do
    with macro-Evolution?

  10. 10
    DATCG says:

    Hello, good to see you. Hope you’ve been well 🙂

  11. 11
    jerry says:

    you’re stating JUNK DNA has nothing to do
    with macro-Evolution


    Or any other part of the DNA genome. Body plans lie somewhere else. No one is sure where but no one is looking at it very hard because nearly everyone in evolutionists biology assumes it is in the genome.

    Johnathan Wells has long thought this and is last two books so has Stephen Meyer. I also suggest everyone read one of Stephen Blume’s books on the impossibility of body plan information being in the genome.

    The followers of Stephen Gould believe that Junk DNA is the source for novel protein development but really have no evidence to back up their beliefs except for speculation. This would be the only way for Darwinian evolution to take place.

    It’s a testable hypothesis and they have not shown it. Doug Axe has shown the mathematical impossibility of proteins forming this way.

    Darwinian processes work just fine in genetics and are important but this produces minor changes only. Or as Robert Sheldon said – #4 in theory acceptance.

  12. 12
    jerry says:

    About 7 months ago Jordan Peterson Tweeted that he had read Stephen Meyer’s new book. I commented that Peterson did not really understand Meyer.


    Meyer answered Peterson with the following reply

    Yes. Microevolutionary processes are observed & well-documented. Mutation & selection are real processes, but lack the creative power to produce the information needed to generate novel protein folds, or major morphological innovations. ~SM

  13. 13
    DATCG says:

    OK, just making sure I understood you 🙂
    Hmmm Architecture Design Plans.
    Found regulatory lncRNAs from 2021 paper with known genes and proteins.
    It’s not specific to body plans but mentions some novel genes found.
    How do you print 3D plots? Funneling building material to supply eventual form?
    Maybe it’s a combo of regulatory features w/proteins and other tag/data features combined.
    Like building a home. Multiple contractors supplying material from inside and outside of home.
    I’m guessing there are unknown regulators yet to be found from the ignored Epigenome of the past.


  14. 14
    DATCG says:

    Agree with what Stephen said. Maybe this sounds silly or stretching a bit. Seems to me skeletal formation measurements would be supplied by regulators and modulators w/measured outcomes.
    Regulators and constructors need constant signal processing ability of formation data.
    If a 3D printer can do it, then it becomes a matter of miniaturization on cellular scale?
    Thinking of nanobots maybe is a way to look at it. We just have not discovered it yet.
    Maybe one way for discovery is to search for regulators that become mutated, causing bone excess
    or deformity.

    Will check in tomorrow.

  15. 15
    jerry says:

    From Stephen Blume’s The DNA Delusion: The Evo-illusion of DNA

    Consider, for example, your body’s crowning glory, your head. How did the bone cells in your skull know enough to marshal themselves into a dome, while those in your jaw formed a trap-shaped mandible? And how did those on your left side arrange themselves in a mirror image of your right, and how were holes left in just the right places for your eyes? Come to think of it, how did your head wind up at the top of your body, nodding sagely at the end of your neck and spine? … How did that blob-like egg give rise to, say, nerve cells in your fingertips with long filaments to cable signals back toward the spine? What informed them to relay their signals to intermediary nerve cells thereby zapping them with chemicals? What told those cells’ filaments to twine themselves into a cord inside your spine, levitate toward your skull, and send messages into the folds of your brain for interpretation

    There are just too many fine constructions (millions of them) that would require exponentially more data than what is available in genome.

  16. 16
    DATCG says:

    Thanks, will look up Blume’s book. Don’t believe macro-evolution counts as “endless forms most beautiful”.
    I do think (maybe) instruction sets exist in the epigenome and wonder how much information and function has yet to be discovered in epigenetic regions.

    Maybe Repair functions can shed some light on the subject? Albeit an easier subset of form. Could similar epigenetic regulators involved in repair exist at birth and initial form shaping?

    Simple Skin repair. Short video…

    Simple Bone repair explanation video…

    Simple Initial bone growth explanation video…

    Looking at videos they show some similar cellular activity and regulation.
    Bone or Skin repair are filling in. They hit stopping points due to surroundings and signal processing as regulation stops repair.

    On initial bone growth during embryonic development the form shape is “unknown”? Or are there instructions rules/sets in epigenetic regulators? Used to monitor initial growth patterns? And can repair epigenetic features be connected to embryonic features of growth?

    Just thinking thru this process using epigenetic factors as logical control systems.

    Here is a paper on regulation of bone and related diseases…

  17. 17
    DATCG says:

    and more “non-coded” RNA processing, may be more relevant…
    The role of microRNAs in bone development

  18. 18
    DATCG says:

    Ha! oh my gosh, reading thru microRNA article in above comment #17.

    Coded Regulators, incredible how this is addressed like any other Code structure in the paper. Any coder reading this paper would say – that’s code! And I love they’re located in introns 🙂 ha! Storage facility. Remember, introns had no function – they’re just discarded junk. Turns out they store information for coding
    Regulators. This is cool use of integration techniques. I’m guessing the storage location is optimized for retrieval purposes. And it must be easily IDed. Maybe a tag identifier.

    From the above paper in 17 on Role of microRNAs in Bone Development…

    Since the first discovery of a miRNA in Caenorhabditis elegans over 25 years ago [23], many more have now been identified in cells of humans, rodents, flies, viruses, plants and other species. In the current miRBase website (http://www.mirbase.org), 1917 mature miRNAs have been identified in humans and 1234 in mice. Mature non-coding miRNAs are commonly 19–24 nucleotides (nt) in length and are derived from larger precursor RNAs.

    Introns storing code…

    Genes encoding miRNAs (predominantly located in intergenic regions or within introns of protein-coding genes) are first transcribed as large primary precursors (pri-miRNAs). In some cases, miRNA-encoding genes may be clustered (i.e. adjacently located within 10 Kb of each other as per miRBase definition) and transcribed in a polycistronic manner.

    Processing calls…

    Primary miRNA transcripts are processed in the nucleus by a Drosha-containing complex and the resulting precursor miRNAs (pre-miRNA) are transported to the cytoplasm and processed further by a Dicer-containing complex to form a short, mature miRNA duplex containing a 5p and 3p strand [24]. Commonly, one of these strands is functional whereby it will bind via its seed sequence (positions 2–8 of the mature miRNA strand) to a complementary region within the 3?UTR of a target mRNA. This interaction occurs within the RNA-induced silencing complex (RISC), the end result being either degradation of the target mRNA or inhibition of mRNA translation [25,26].

    60% of protein-coding genes ‘may’ be modulated by miRNAs…

    Although miRNAs account for only 1–5% of the human genome [29], up to 60% of protein-coding genes may be modulated by miRNAs [30] thereby rendering these non-coding RNAs as major epigenetic regulators in the cell. While the majority of miRNAs carry out their function in the cytoplasm, many miRNAs have also been localized to other organelles including the nucleoli, processing bodies and mitochondria [31]. It has also been demonstrated that miRNAs can exist inside extracellular vesicles such as exosomes and that cells can communicate with each other via exosomal delivery of miRNAs [32,33]. Overall, a massive body of published research indicates that miRNAs play important roles in development, homeostasis, turnover, disease and repair of many different tissue types. Specifically, miRNAs have been shown to regulate a wide range of cellular processes including proliferation, cytoskeleton formation, apoptosis, growth factor signaling, metabolism, cell differentiation, and many others.

    Amazing 🙂

  19. 19
    jerry says:

    may be more relevant

    You are pointing to extremely clever controls in the genome. Whether there are enough of these to precisely place each cell in a developing fetus is a question to be researched.

    The place to research this is with non-human genomes which are of various sizes and often have very different non-coding parts to their genome.

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