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.

Now it has always been thought that epigenetic mechanisms happen only in “highly-evolved” organisms. After all, “primitive” organisms are not thought to have complex DNA mechanisms, because those mechanisms never evolved in such organisms. That’s where the big news comes in. A team of researchers at the University of Nebraska-Lincoln recently published a paper in which they demonstrate that a “primitive” bacterium (Sulfolobus solfataricus) has epigenetic mechanisms!

This bacterium lives in the hot, sulfur-rich waters of places like the Grand Prismatic Spring shown above. Such bacteria are assumed to be among the first living cells that evolved, so they are thought to represent life at its most primitive. The researchers decided to start exposing the bacteria to higher levels of acid, trying to see if the bacteria could increase their acid resistance. They found that over time, the bacteria could increase acid resistance by almost 200x what they have in the wild. Some of them did it by altering the sequence of their DNA through mutations, but one group of bacteria increased their acid resistance without changing their DNA sequence at all. Thus, they became acid resistant through epigenetic means, not through mutation!

Dr. Paul Blum, one of the scientists involved in the research, put it this way:

The surprise is that it’s in these relatively primitive organisms, which we know to be ancient…We’ve been thinking about this as something (evolutionarily) new. But epigenetics is not a newcomer to the planet.

Of course it’s not new to the planet. Complex mechanisms don’t evolve. They are designed. Anything as complex as epigenetics must be a part of the original design of creation. Thus, it’s not surprising to find it in even the “simplest” life forms on the planet.

This discovery emphasizes something that I tell my students over and over again in my biology book: There is no such thing as a simple life form. Even at its most basic level, life is mind-bogglingly complex!

26 Comments

  1. Jim Pemberton says:

    This is fascinating stuff. It seems the more we learn, the more we find we don’t know. What I see here is further depth to the level of complexity of the genetic system and possibly some answers to the specialization of cells in complex organisms, especially in the early development of the organism.

    Am I to understand that these epigenetic mechanisms do not alter DNA sequences, but somehow can pass additional information from parent to child? Is it in the mDNA or somewhere else? So we know that mDNA has some kind of change over time. How does this affect the argumentation regarding evolution, particularly with speciation within a genome versus genetic drift of populations into new genomes?

    1. Jay Wile says:

      This has nothing to do with mitochondrial DNA. This is all about the DNA found in the nucleus, which is nuclear DNA. You are right that information is being passed down in a way that does not alter DNA sequences. Epigenetics relates to evolution mostly because it tells us that the environment can, indeed, shape what is passed on to the children. So it’s not just mutation that causes changes in traits. It’s also epigenetic mechanisms that are triggered by the environment. This is not exactly like Lamarkian evolution, but many have said is is quite similar.

      1. John D says:

        Dr. Wile, in the above comment you say “This is not exactly like Lamarkian evolution”, and I recall in some other articles that you seem very hesitant to suggest that various processes are Lamarkian. Do you think this is somewhat unfair? Darwin was not alive long enough to offer or embrace the Neo Darwinian random mutation/selection mechanism, but I don’t believe I hear scientists suggest that the process is “not exactly Darwin” (although maybe some do?).

        I suppose I can see where you’re coming from in that (so far as we know) epigentics has not yet been determined to author DNA (rather governing its expression or lack thereof).

        But when you consider Lamarck in light of new epigentic research AND contemporary studies which suggest mutations occur more often when they are advantageous to the organism (prior to any selective pressure), doesn’t it seem like he deserves a new hearing? It seems, much like Lamarck suggested, that pressure from the environment instigates change in the organism (today we see this via many processes including point mutations, methylation, etc) and then use/disuse (with some help from natural selection) fixes these changes into the population. I’m referencing this study http://www.genetics.org/content/126/1/5.long and also thinking of various replicable beneficial mutation studies like Lenki’s yeast living on citrate (interestingly the citrate digesting benefit was achieved through different point mutations in different trials.)

        I know when I was in school Lamarck was paraded as sort of a “don’t make this mistake” figure. I think it’s because if Lamarck is right then natural selection is demoted to a secondary filter, the agent of increasing fitness is no longer random mutation, and furthermore – Lamarck believed God authored the universe (although Lamarck believed in sort of a “hands off” God ). I’m wondering if maybe you have some of that old “institutional dust” you need to shake from your heels when it comes to Lamarck.

        Anyways, thanks as always for these thought provoking articles. They really do keep me interested in this stuff. John

        1. Jay Wile says:

          I see where you’re coming from, John. I guess the reason I am saying it’s not exactly Lamarckian is because Lamarck thought that the change originated from effort. If a horse strained its neck, it produced offspring with longer necks. If it ran a lot, it produced offspring with more muscular legs. So it was “improvement by effort.” The changes we see happening today are either pre-programmed mutations in response to a stimulus or an epigenetic change that is probably a reaction to the environment. When the bacteria in Lenski’s experiment became able to eat citrate in an oxygen environment, it wasn’t because they tried to eat citrate and that effort changed them. It was because starvation stress triggered a pre-programmed mutation that broke the citrate regulating system. When an epigenetic change is inherited (like the Mexican blind cave fish), it’s probably not because the eyes weren’t being used. It was probably a response to the prolonged darkness.

          At the same time, I do agree that we shouldn’t parade Lamarck around as a “don’t make this mistake” example.

  2. Tomi Aalto says:

    I’m glad that you have now understood that DNA doesn’t determine traits as I said about two years ago when making comments on your articles. Please take a look at my blog articles that handle this same issue:
    https://sciencerefutesevolution.blogspot.com/2019/01/its-end-of-gene-as-you-know-it.html
    https://sciencerefutesevolution.blogspot.com/2017/06/the-entire-concept-of-gene-has-to-be.html
    https://sciencerefutesevolution.blogspot.com/2018/09/lactose-tolerance-is-regulated-by.html

    1. Jay Wile says:

      As I told you back then, Tomi, we can definitely connect some traits to gene sequences. Sickle-cell anemia is a trait, for example, and it can be directly linked to a specific variation in the sequence of the gene that codes for hemoglobin. I certainly agree that there is a lot more to a person than his or her genes, but there are traits in people that can be linked to specific gene sequences. This is even more the case for less-complex organisms, like the fruit fly. Eye color, body color, and many other traits have been directly linked to the sequence of specific genes in the fruit fly. Indeed, the way epigenetics affects traits is by regulating what the genes do. That is, in fact, exactly what the articles your blog posts are based on say. So without the process by which gene sequences shape traits, epigenetics would be useless.

      1. Tomi Aalto says:

        Wrong. Eye color is so called polygenic trait. Modern science is starting to understand that it is regulated by epigenetic factors. There is no active DNA strand without epigenetic control. There is no active protein without methylation. The sickle cell mutation is not necessarily harmful if the mutation is located on an inactive DNA section. There are two sets of so called genes in diploid organisms. Only the other one of those two ‘genes’ can be at use. The other one one is silenced. This is done by epigenetic mechanisms, too.

        But I don’t want to be annoying. I understand your view and maybe the term ‘trait’ is not ideal when talking about determination of biological information. Maybe I should use a term ‘characteristics’ instead. Ideas?

        1. Jay Wile says:

          Yes, eye color is a polygenetic trait. Which means it is determined by the sequences of multiple genes. Thus, the genes determine the trait. You can learn about the genetics of eye color here. Note that epigenetics plays no role. Sickle cell anemia alleles are never deactivated. If you have one recessive allele, half of your red blood cells are sickle shaped, because that allele produces sickle cells. If you have two recessive alleles, all your cells are sickle shaped. You can learn about that here. Once again, note how epigenetics plays no role.

          You need to review your genetics, because you aren’t correct. There are two alleles for every gene in a diploid organism. In many of those genes, one allele is dominant, and the other is recessive. As a result, the dominant allele determines the trait. This has nothing to do with epigenetics. In many cases, some alleles are codominant over others. For example, in human blood type, there are three possible alleles to determine the letter of your blood type: A, B, and O. A and B dominate over O, but not over each other. Thus, if you have the A and O alleles, you are type A. If you have the B and O alleles, you are type B. If you have the A and B alleles, you are type AB. This is because the A allele makes A-type antigens on your red blood cells, the B allele makes B-type antigens, and the O allele makes no antigen. The body uses both alleles, so if you have A and O, your body makes A-type antigens and no antigens. Same with B and O. With A and B, however, since both alleles are used, your body makes both A and B antigens on your red blood cells. You can learn more about that here. Once again, note that epigenetics plays no role.

          Yes, epigenetics is important, but it doesn’t change the fact that traits are mostly determined by genes.

        2. Tomi Aalto says:

          Blood type determination is not that simple. “The ‘O’ blood group is caused by a deletion of guanine-258 near the N-terminus of the protein which results in a frameshift and translation of an almost entirely different protein. Individuals with the A, B, and AB alleles express glycosyltransferase activities that convert the H antigen into the A or B antigen.”

          Amino acid deletions and substitutions in proteins are caused by differences in alternative splicing mechanism which is controlled by epigenetic mechanisms.

          Don’t you know that genetically identical monozygotic twins might have different blood types, eye colors, hair and skin colors?

          DNA is just passive form of biological information and it has no control over cellular processes. Even some respectful evolutionary biologists, like Denis Noble, understand this biological fact.

          Keywords: Denis Noble DNA passive data base

        3. Jay Wile says:

          Tomi, you really need to review this, because amino acid deletions and substitutions are not caused by epigenetic mechanisms. They don’t even fit the definition of epigenetics, since a deletion or substitution affects the sequence of the gene. You can go here to see the differences in sequences between the A, B, and O alleles. Since the differences are in the sequences of the alleles, it’s not epigenetics. It’s genetics.

          Yes, identical twins can have slightly different eye color, but the differences are subtle. Those are, indeed, caused by epigenetic mechanisms. For example, because of one twin’s environment, the DNA may be regulated to cause more uptake of melanin, making a slightly darker color. However, the base color is fixed by the sequence of the genes. The shade of that color can be influenced by epigenetic mechanisms. Now, it is possible for monozygotic twins to have remarkably different traits, but that is because of somatic point mutations that happen early in development. Those mutations can cause a change in the sequence of one twin’s genes. Of course, at that point, the twins are not genetically identical anymore. If gene sequences don’t cause traits, why does it take a change in gene sequence (as discussed in that paper) to cause remarkably different traits in monozygotic twins?

          I think you need to spend more time reading Dr. Noble. Yes, he says that there is more to biology than gene sequences. However, he does not discount that gene sequences determine traits. He just says that the effects are buffered by other networks of interactions and by epigenetic mechanisms. Look, for example, at Figure 1 in his 2011 Journal of Physiology paper. The base is DNA sequence. The biological networks affect how the information in those sequences is used, but the sequence is the starting place, because the sequence determines the trait. As he says here:

          A DNA sequence only makes sense in the context of particular organisms in which it is involved in phenotypic characteristics which can be selected for. A sequence that may be very successful in one organism and/or environment, might be lethal in another.

          How could a sequence be successful in one organism and lethal in another if the gene sequence doesn’t determine the trait?

          Perhaps it’s statements like the following sentence that confuse you:

          This is evident in the fact that almost all cross-species clones do not form an adult (see later for an important exception). The same, or similar, DNA sequence may contribute to different, even unrelated, functions in different species. The sequence, intrinsically, is neutral with regard to such functional questions.

          What he is talking about here (as he says repeatedly in his paper) is that Dawkins’s idea of the “selfish gene” is silly. Of course, any reasonable biologist already knows that. He is simply saying that the sequence itself means nothing except in the context of an organism. The gene sequence that produces hemoglobin, for example, means nothing in an organism that doesn’t use hemoglobin. This doesn’t mean the sequence is unimportant. In fact, he understands that it is the basis of the trait, as he shows in Figure 1.

        4. Tomi Aalto says:

          //There are two alleles for every gene in a diploid organism. In many of those genes, one allele is dominant, and the other is recessive. As a result, the dominant allele determines the trait. This has nothing to do with epigenetics.//

          According to the latest research, that’s not true. Please have a look at this video made by Gregg Lab:

          https://www.youtube.com/watch?v=GfIvZIy1uDc

          You should know that turning genes on or off is done by epigenetic mechanisms and factors.

          About the blood types. Blood types are strongly associated with properly functioning immune system and if there are three genetic markers determining those basic three blood types, then those markers are accurately controlled by the immune system and by mechanisms it regulates such as AID mediated deamination. Genetic variants (mutations) in the ABO gene are associated with serious diseases:

          https://www.ncbi.nlm.nih.gov/pubmed/26924317

          There are several complex mechanisms regulating mRNA processing such as alternative splicing and RNA-A-to-I editing. They are so accurate mechanisms that only intentional changes in the DNA can result in successful mRNA:s and proteins.

          http://www.biology-pages.info/R/RNA_Editing.html

          There is an ABO sequence in a stem cell. Why doesn’t it produce any protein?
          There are HERC2, OCA2 and SLC45A sequences in the human stem cell. Why don’t they produce any pigment?

        5. Jay Wile says:

          Once again, Tomi, you need to spend more time studying this. The video you gave me makes it very clear that the turning off of one allele happens in only some cells. As the video itself says, “A subpopulation of cells in the body express only one of the two copies, and the other copy is turned off.” The rest work exactly as standard genetic says. Both alleles are used. Yes, the turning off of one allele is epigenetic. However, as the video says, it happens in a subpopulation of cells.

          Also, note what the video says results from this: “Some cells in the body are especially vulnerable to the effects of mutations because they turned off their healthy gene copy.” Now, if gene sequences didn’t determine traits, why would a mutation in the sequence of the one allele that is turned on cause them to be vulnerable to the disease?

          Once again, you don’t seem to understand blood type. The fact is there is nothing epigenetics can do about the letter type of your blood, because the body uses both alleles. Thus, if you have one A allele and one B allele, your red blood cells will be AB. This is, once again, because the body uses both alleles. Neither is turned off.

          Indeed, the link you gave once again underscores how the sequence of a gene determines the trait. It traces mutations in the gene that determines blood type (once again, the sequence determines the blood type) and finds that specific mutations increase the person’s risk of LAA stroke. Now, if gene sequence doesn’t cause traits, why would a change in sequence cause an increase in stroke risk?

          Yes, alternative splicing does exist. I have written about it on a couple of occasions (see here and here). I have also written about RNA editing (see here and here). Once again, both of those processes alter the sequence of the mRNA before it becomes a protein. This, once again, underscores the important of the sequence of the gene.

          Yes, stem cells don’t express certain genes, because the cells haven’t differentiated yet. The differentiation process uses epigenetic means to turn on certain genes and turn off certain genes in order to make the cell do what it is supposed to end up doing. However, that once again underscores the importance of the gene sequence. If the sequence wasn’t important, it wouldn’t matter whether or not the gene was turned on or turned off. Blood type is a great example of this. If the cell is not a red blood cell, the ABO gene is never turned on. However, if the cell differentiates into a red blood cell, the ABO gene is turned on, and when that happens, both alleles are turned on. This is why we have type AB blood. If the person has an A allele and a B allele, both are turned on for all red blood cells, and as a result, all red blood cells have A and B antigens on it.

          It’s the same with sickle cell anemia. If the stem cell doesn’t become a red blood cell, the hemoglobin gene is not turned on. If the cell differentiates into a red blood cell, then both alleles of the gene are turned on. As a result, if the person has one normal allele and one sickle allele, half of the red blood cells will be sickle. If the person has two sickle alleles, all the red blood cells will be sickle. Once again, both alleles are turned on when the gene is turned on, and the sequence of each allele determines the types of red blood cell made.

          I am really glad that you are interested in all of this, but you need to study the issue a lot more.

        6. Tomi Aalto says:

          DNA is just passive form of biological information and it has no control over cellular processes. A stem cell has an entire genome with all the same DNA sequences as a differentiated cell has but it does nothing without epigenetic control.

          DNA is needed for the cell being able to build functional RNA molecules by reading the DNA. Reading and transcription is guided by several epigenetic mechanisms, such as DNA methylation profiles, histone epigenetic markers and non coding RNA molecules. No strand of DNA gets into transcription without epigenetic control. The DNA is needed for production of proteins but also for a wide variety of non coding RNA molecules that transfer epigenetic markers (over 140 of different types) between cells and between the environment and the cells. RNA molecules have significant tasks in transgenerational epigenetic inheritance. For example, there are thousands of different lncRNAs, miRNAs and other ncRNAs in human sperm (vesicles) that transfer epigenetic information for developing embryo. They are needed for epigenetic reprogamming and especially for the establisment of the histone code of the embryo.

          DNA doesn’t determine characteristics. Think about a butterfly metamorphosis. In all four stages the DNA is the same. Epigenetic mechanisms control what sections of the DNA are read into transcription at accurate timing. This is modulated by diet type and developmental phase.

          https://sciencerefutesevolution.blogspot.com/2018/09/dna-doesnt-determine-phenotype-or.html

          Excerpt: “Surprisingly, however, the number of vertebrae in the clones was that of the species providing the recipient egg. Thus the egg cytoplasm, and not the genetic code of the transplanted nucleus, affected this skeletal characteristic in the offspring.”

          This is a great example of how the cell uses DNA material. DNA has no control over cellular processes, phenotypes, individual characteristics or body plan. Epigenetic reprogramming of stem cells is needed for embryonic development. This complex reprogramming procedure is mediated by non coding RNA molecules that transfer necessary epigenetic markers for histone tails and DNA bases (cytosine and adenine methylation). There is no such thing as mutation driven evolution. Variation of organisms is based on epigenetic regulation of existing biological information and it will never lead to any kind of evolution.

        7. Jay Wile says:

          Yes, a stem cell has the entire genome, and epigenetics determines which genes are turned on and which are turned off. That is part of the differentiation process. However, that doesn’t take away from the fact that gene sequences determine traits. As I have already tried to explain to you, when a cell differentiates into a red blood cell, the genes needed to make it a red blood cell are turned on, and the unnecessary genes are turned off. That’s epigenetics. After that, it’s genetics. The sequence of each allele determines the traits of the red blood cell. An A allele produces A-antigens on the surface of the blood cell, and a B allele produces B-antigens on the surface of the red blood cell. This is all determined by the sequence of each allele. Thus, gene sequence determines trait. Same with sickle cell disease. When the hemoglobin gene is turned on, the sequence of the gene determines the shape of the red blood cell. Since both alleles of the gene are used, if the sequence of one allele causes sickle cells, then half of the cells will be sickle. If the sequences of both alleles causes sickle cells, then all the red blood cells are sickle. Thus, the sequence determine the trait.

          Yes, epigenetics directs the metamorphosis of a butterfly. However, all insects go through metamorphosis. What makes a butterfly’s metamorphosis different from a housefly’s metamorphosis? The sequence of the genes in the genome. Once again, then, while epigenetics is important, it does not determine traits. It interprets the DNA based on the organism’s needs, but it does not determine traits. The sequence of genes determines traits. Epigenetics simply modulates the results. This is exactly what Dr. Noble is saying in his work, and it’s exactly what science is showing us.

          Perhaps this article will help clear up your confusion. They give a good summation of what epigenetics does:

          Epigenetics can be thought of as the interpretation of the genetic code. Just as the same piece of music will change slightly when interpreted by different orchestras, so does our genetic ‘score’ when interpreted by the epigenetic orchestra.

          That’s exactly the point. Traits are determined by genes. Epigenetics decides when those traits are important, and it can modulate those traits a bit. The score of the music determines the traits of the piece. The interpretation of the music gives the nuances of the performance. Once again, this is why identical twins can have slight variations, but to get a marked difference between monozygous twins, there must be a somatic mutation, which changes the sequence of a gene. At that point, the twins are no longer genetically identical.

        8. Tomi Aalto says:

          //Tomi, you really need to review this, because amino acid deletions and substitutions are not caused by epigenetic mechanisms.//

          I think you need to update your knowledge about epigenetic mechanisms:

          https://bmcgenomics.biomedcentral.com/articles/10.1186/s12864-017-4409-8

          “Adenosine-to-inosine (A-to-I) RNA editing is an epigenetic modification catalyzed by adenosine deaminases acting on RNA (ADARs)…”

          https://www.mdanderson.org/newsroom/rna-editing-study-shows-potential-for-more-effective-precision-cancer-treatment.h00-159223356.html

          “The researchers demonstrated how A-to-I RNA editing contributes to protein diversity in breast cancer by making changes in amino acid sequences. They found one protein, known as coatomer subunit alpha (COPA), increased cancer cell proliferation, migration and invasion in vitro, following A-to-I RNA editing.”

        9. Jay Wile says:

          I think you need to learn some basic definitions in biology. Amino acid deletions and substitutions are not a part of RNA editing. They are mutations that occur in the sequence of the DNA. That’s why they can strongly affect the organism. They change the sequence of a gene, which changes a trait. RNA editing is, indeed, an epigenetic process, but it has nothing to do with amino acid deletions and substitutions. It can change the amino acids in a protein, but it is not what “amino acid deletion” and “amino acid substitution” refers to.

          I have to point out here that you raised the subject of amino acid deletions and substitutions when you were trying to interpret blood type based on epigenetics. As I showed you, it has nothing to do with epigenetics. The actual sequences of the ABO gene alleles are different, which is what causes the different blood types. Once again, it’s gene sequence, not epigenetics.

        10. Tomi Aalto says:

          //I think you need to learn some basic definitions in biology. Amino acid deletions and substitutions are not a part of RNA editing. They are mutations that occur in the sequence of the DNA.//

          https://www.ncbi.nlm.nih.gov/pubmed/22271460

          “RNA editing is one of the post-transcriptional RNA processes. RNA editing generates RNA and protein diversity in eukaryotes and results in specific amino acid substitutions, deletions, and changes in gene expression levels. Adenosine-to-inosine RNA editing represents the most important class of editing in human and affects function of many genes. The importance of balancing RNA modification levels across time and space is becoming increasingly evident. In this review, we overview the biological significance of RNA editing including RNA editing in tumorigenesis, RNA editing in neuronal tissues, RNA editing as a regulator of gene expression, and RNA editing in dsRNA-mediated gene silencing, which may increase our understanding of RNA biology.”

          I think you are talking about base pair substitutions. Amino acids are needed for building up proteins. There are several reasons for why amino acids might substitute:

          – Base pair alterations (mutations)
          – Alternative splicing
          – RNA A-to-I editing
          – RNA G-to-A editing
          – AID mediated deamination

          I think you have seriously misunderstood the role of the DNA in the cell. I repeat, the DNA is just passive form of biological information and it has no control over cellular processes. One strand of DNA can be used for several purposes (multifunctional genes). A so called ‘gene’ can be located in more than one strand of the DNA. Strands can be read even from different chromosomes. They can be embedded, overlapped and stay in both 5′ and 3′ directions.

          You know that alternative splicing makes it possible for the cell to produce thousands of different mRNAs by using only one (or combined ones) section of the DNA. Editing and modification is done at RNA level. The main purpose of the DNA is to make it possible for the cell to build functional RNA molecules. There’s the real code of life.

          Multifunctional DNA strands regarding protein encoding DNA mean that the DNA is so cleverly designed and optimized that it doesn’t tolerate mutations. That’s why mutations typically result in genetic diseases.

        11. Jay Wile says:

          Once again, Tomi, the amino acid deletions and substitutions that you brought up were in reference to blood type, and they refer to sequence changes, not epigenetics. I will quote you:

          Blood type determination is not that simple. “The ‘O’ blood group is caused by a deletion of guanine-258 near the N-terminus of the protein which results in a frameshift and translation of an almost entirely different protein. Individuals with the A, B, and AB alleles express glycosyltransferase activities that convert the H antigen into the A or B antigen.”

          Amino acid deletions and substitutions in proteins are caused by differences in alternative splicing mechanism which is controlled by epigenetic mechanisms.

          That is false. The O-blood type allele is not caused by alternative splicing or epigenetic mechanisms. As I showed you already, it is a different sequence than the A allele and B allele. Once again, learn the basic terms of biology.

          You really need to read the article I linked so that you understand what epigenetics is. As the article attempts to teach the reader, and as the science we know currently understands, the sequence of the genes determines traits. Epigentics can modify the traits, but the gene sequences are what cause the traits. This is why the article likens DNA to the score and epigenetics to the orchestra. The orchestra can add nuances to the piece, but the piece is determined by the score. In the same way, DNA determines the traits. Epigenetics adds nuances to those traits.

          If gene sequences don’t cause traits, why are there blood types? Why does someone with one “A” allele and one “B” allele have A and B antigens on his or her cells? Why does someone with the “A” allele and the “O” allele have only A antigens on the red blood cells? Why does someone with two “O” alleles have none of those antigens on the red blood cells? The sequences determine those traits. Yes, there is a lot more to it than just the genes (as the article I am trying to get you to read indicates), but the sequences of the genes are the basis.

          Identical twins are the best illustration of the relationship between gene sequences and epigenetics. Identical twins look nearly identical, because their gene sequences are the most important part of trait determination. They are slightly different because of epigenetics. That shows you the relative importance of the two: gene sequences do most of the determination, epigenetics does the nuances.

        12. Tomi Aalto says:

          Dr Wile, I appreciate that you have published every comment we have written to each other. This conversation has been very interesting. For several years I have studied how epigenetic factors and mechanisms affect biodiversity. Now I want to show you a few examples of the power of epigenetics. I wish you take some time and read them carefully.

          1. The Italian wall lizard. Major changes in morphology, behaviour and especially a ‘new’ structure in its gut, Cecal valve. No genetic alterations were associated with these changes. The reason is the diet type from insects to plants that modulated the epigenome.

          https://sciencerefutesevolution.blogspot.com/2016/12/can-evolution-produce-new-structures.html
          https://sciencerefutesevolution.blogspot.com/2016/11/plant-micrornas-play-role-in-gene.html
          https://journals.plos.org/plosone/article?id=10.1371%2Fjournal.pone.0185227&fbclid=IwAR3VoiIOh4RbI8lyYVG-oGUZv31cOcOGx0SU00xZ6YXyL56ZOspvBQq6oTU

          2. Darwin’s finches. Even secular science admits that changes in their morphological traits were due to epigenetic control of gene expression.

          https://sciencerefutesevolution.blogspot.com/2017/08/distinct-diets-explain-differences.html

          3. Lactose tolerance.

          https://sciencerefutesevolution.blogspot.com/2018/09/lactose-tolerance-is-regulated-by.html

          4. Human traits.

          https://sciencerefutesevolution.blogspot.com/2017/03/human-traits-and-epigenetics.html
          https://sciencerefutesevolution.blogspot.com/2017/07/the-epigenetics-behind-unique-human.html

          5. Plant variation.

          https://sciencerefutesevolution.blogspot.com/2017/06/not-evolution-but-epigenetic-variation.html

          6. Honeybee phenotype

          https://sciencerefutesevolution.blogspot.com/2018/09/same-genome-can-yield-very-different.html

          7. Ant phenotype

          https://sciencerefutesevolution.blogspot.com/2018/10/a-soldier-or-worker-ant-epigenetic.html

          8. Blind cave fish

          https://sciencerefutesevolution.blogspot.com/2017/04/how-millions-of-years-changed-to.html

          A few words about the concept of ‘a gene’. Serious scientists want to move it to RNA side. Here’s why:

          https://sciencerefutesevolution.blogspot.com/2017/06/the-entire-concept-of-gene-has-to-be.html
          https://sciencerefutesevolution.blogspot.com/2018/03/the-dna-gene-is-dead.html
          https://sciencerefutesevolution.blogspot.com/2018/08/the-central-term-of-genetics-genecan-no.html
          https://sciencerefutesevolution.blogspot.com/2019/01/its-end-of-gene-as-you-know-it.html

          “For years, disappointment followed: Only a few extremely weak associations between SNPs and observable human characteristics could be found.”

          Some of those weak associations are linked to those blood groups that can be predicted by SNPs in the ABO gene. But because that ‘gene’ needs to be expressed in order to be transcribed and the transcription will be modified and accurately checked by several RNA-level mechanisms, I would say that those SNPs are written by the immune system. Blood groups are very important and they have a vital immunological function. They help us fight diseases. The cell is able to modify both DNA and especially RNA.

          God bless You, Dr Wile!

        13. Jay Wile says:

          I have been trying to educate you on this issue, Tomi, but I have to say that it is frustrating sometimes. You tend to ignore anything that demonstrates your view to be incorrect. Blood types are a good example. You claim they are “weak associations” that are “written by the immune system.” But that is just wrong. They are not “weak associations.” If you receive blood with an incompatible type, you die. That is anything but a “weak association!” Where do the blood types come from? Not from the immune system. I showed you the link twice before, but I will show it to you one more time. We know the sequences of the variants of the ABO gene, and we can show that all the differences between blood types are directly the result of the differences in the sequences on those alleles. There is simply no role that epigenetics plays in blood type. I understand the excitement that epigenetics has added to the field, but that doesn’t mean it is anywhere near as important as you think it is.

          As for the links you share, none of these studies are new to me. Indeed, I discussed lactose tolerance in this post, and I have linked to you my discussion on blind cave fish. In addition, in my article on Italian wall lizards, I make it clear that the cecal valve is not a new structure and I give the epigenetic reason that it appears in these lizards:

          However, it’s not really a brand-new structure. As the scientific article says:

          “These valves are similar in overall appearance and structure to those found in herbivorous lacertid, agamid, and iguanid lizards and are not found in other populations of P. sicula or in P. melisellensis.”

          So in fact, the cecal valves are not “brand-new” structures. They exist in other lizards. However, they are brand-new for this species, and perhaps even for the genus. Now remember, these cecal valves have appeared in these lizards since 1971, which was only 37 years before the study. The idea that these lizards could produce a completely new structure that quickly is rather hard to believe. I think a more likely explanation is that the genes necessary for the production of cecal valves were already in the genome of these lizards, but they were “turned off” because they were not needed. When the lizards were put in an environment where cecal valves were needed, the genes were “turned on” again, producing cecal valves.

          What you don’t seem to appreciate is that epigenetics does not make the cecal valve. The sequence on the genes makes the cecal valve. Epigenetics just turned the genes on so the sequence on the genes could do its job.

          Your discussion of the concept of ‘gene’ brings up another point. Your commentary on the articles you post often mischaracterizes what the actual article says by leaving out key facts. For example, you comment on this article and in your comments, you leave out the focus of the article: their newly-proposed definition of a gene. Here is what they propose:

          A gene is a DNA sequence (whose component segments do not necessarily need to be physically contiguous) that specifies one or more sequence-related RNAs/proteins that are both evoked by GRNs and participate as elements in GRNs, often with indirect effects, or as outputs of GRNs, the latter yielding more direct phenotypic effects. (emphasis mine)

          Their definition, the focus of the article which you don’t even mention in your comments, clearly references the sequence of the gene as either indirectly or directly affecting traits (phenotype). Once again, then, even the articles on which you comment demonstrate that your idea that gene sequence doesn’t determine traits is wrong.

          Please note that I will not publish any more comments from you unless you answer this question. Please think about it carefully:

          If epigenetics is what determines traits, why are identical twins (even ones raised separately) so very similar in their traits? They have identical sequences in their DNA, but different epigenetics. Nevertheless, they are nearly identical.

          Now, of course, some pairs of monozygous twins can have remarkable differences, but as I have already told you, those differences can be traced to somatic mutations in DNA sequences that occur early in development. At that point, of course, the twins are not genetically identical.

          As I said previously, identical twins are the best illustration of the relationship between genetics and epigenetics. The sequences in the DNA determine the traits. Epigenetics then modulates the traits a bit. As the article I have been trying to get you to read says: Genetics is the score. Epigenetics is the orchestra. When I hear Beethoven’s Fifth Symphony, I can always recognize it, because the score determines its traits. Every symphony has its own variation, making subtle differences between different performances. In the same way, the sequences in DNA determine the traits, and epigenetics makes the subtle changes, like what you see in identical twins.

        14. Tomi Aalto says:

          //If epigenetics is what determines traits, why are identical twins (even ones raised separately) so very similar in their traits? They have identical sequences in their DNA, but different epigenetics. Nevertheless, they are nearly identical.//

          Please take it easy Dr Wile. I understand it’s difficult to change your way of understanding about how the DNA is used by the cell. It takes some time but it’s worth it. Seems that you didn’t read my links. That’s pity.

          Identical twins, if they share similar characteristics, have similar epigenomes.

          https://www.ncbi.nlm.nih.gov/pubmed/29310692

          But there are very interesting exceptions like this one:

          https://www.dailymail.co.uk/femail/article-3461832/First-identical-twins-different-skin-colour-born-UK.html

          Scientists have not found ‘racial’ genes or SNPs that could be linked to skin color variation. I’m sure that the skin color is regulated by epigenetic factors and mechanisms. Histone markers are often very stable epigenetic information layers and the necessary information for their establisment is transferred by non coding RNA molecules (miRNAs, lncRNAs) in sperm and ovum.

          I didn’t claim that the Cecal valve was a new structure. It was claimed to be new by evolution believers. It was epigenetically switched on due to changed diet. But not by DNA sequences. RNA molecules are needed to transfer the necessary information for DNA activation, chromatin folding and histone markers.

          I can see you are very frustrated because you can’t turn my head to adopt the concept of a gene driven by population genetics. Please remember that I’m a Christian and I don’t believe in mutation driven evolution. I don’t believe in random beneficial mutations. Before you close this thread, I wish you could answer these short questions regarding ABO ‘gene’ and the blood groups:

          1. Why does the ABO ‘gene’ end up into transcription? What mechanisms control the transcription mechanisms to read that sequence? How does the transcription mechanism find the correct sequence?
          2. What does the cell produce when reading the ABO ‘gene’ into transcription?
          3. Is that product modified? By what mechanisms? Why?
          4. How is the integrity and validity of the mature mRNA checked before it is released in the cytoplasm?
          5. Are there other mRNAs produced from the same DNA strand as the ABO mRNA?
          6. Is the ABO ‘gene’ associated with the immune system?

          Kind regards,

          Tomi

        15. Jay Wile says:

          Tomi, as I said, I am trying to educate you on this issue, but you seem unwilling to learn. That makes it very frustrating. I did, indeed, read your links. You can tell that, because I commented on them and even showed you how your commentary misrepresented one of the articles on which it was based. As I showed you, the very article you comment on demonstrates that your ideas are wrong, but you didn’t even seem to notice that. The second link you share in this comment is another perfect example of you not paying attention to what you are reading. As the link clearly says:

          However, an exception might be when a change in one of these genes that control skin colour happens after the twins separate in very early development – so called somatic mutation.

          This is exactly what I have been trying to tell you. When identical twins are markedly different, it is because of sequence changes in the DNA, not because of epigenetics. I have linked the study to you, but characteristically, you ignored it. Also, your other statement about twins is quite false on two counts. You say. “Identical twins, if they share similar characteristics, have similar epigenomes.” First, it’s not a case of if they share similar characteristics. They definitely do share similar characteristics. This is why it is hard to tell identical twins apart. They share very similar characteristics, because of their identical DNA sequences. Second, it’s not because they have similar epigenomes. Once again, the very link you give demonstrates that to be false. As the research article says, this was found only for a small group of genes, many of which are involved with cancer. In addition, they found several genes that had no epigenetic supersimilarity. Thus, this does not explain why identical twins share similarities in all traits.

          Once again, then, I ask you: If epigenetics is more important than gene sequences, why are identical twins nearly identical? As the very article you linked says, epigenetic similarity doesn’t apply to very many genes. Unless you provide a reasonable answer to that question, I will not post another one of your comments.

          You say, “Scientists have not found ‘racial’ genes or SNPs that could be linked to skin color variation.” That, of course, is false. In fact, we know those SNPs so well that we can use them to predict skin color. Skin color variation is well understood, and like nearly every trait, its main influencer is gene sequence, as shown in the linked study.

          I am not a believer in mutation-driven evolution as well. However, as a Christian, I am interested in understanding the truth of God’s creation. As a result, I cannot reject an idea just because I don’t like it. The data are very clear that gene sequences are the main influencer of traits, as identical twins demonstrate. Thus, I have to believe it, whether or not I like it. That’s what it means to be a Christian and a scientist – working to find the truth of God’s creation, regardless of my own personal preferences.

          I am happy to answer your questions. I hope you try to learn from my answers:

          1. Why does the ABO ‘gene’ end up into transcription? What mechanisms control the transcription mechanisms to read that sequence? How does the transcription mechanism find the correct sequence?

          We do not have a full description, but many of the processes are laid out here.

          2. What does the cell produce when reading the ABO ‘gene’ into transcription?

          It produces RNA. The sequence of nucleotide bases on the RNA is determined by the sequence of each allele. Since the body uses both alleles, each allele produces its own RNA.

          3. Is that product modified? By what mechanisms? Why?

          The introns are removed before the DNA leaves the nucleus. This is because the individual sequences can be used to construct other proteins as well.

          4. How is the integrity and validity of the mature mRNA checked before it is released in the cytoplasm?

          A CAP is added to the 5′-end, and a Poly-A chain of adenine nucleotides is added to the 3′-end

          5. Are there other mRNAs produced from the same DNA strand as the ABO mRNA?

          I don’t know. It’s certainly possible that one or more of the exons are spliced together to make a different mRNA. That’s why there are introns, after all.

          6. Is the ABO ‘gene’ associated with the immune system?

          The gene itself? Only as a part of the body’s self-recognition. That’s why the immune system reacts to the antigens that are NOT produced by the gene. If you have the A allele of the ABO gene, your red blood cells produce A-type antigens. If you also have the O allele, it produces no antigens. As a result, your immune system is designed (by the gene sequences that control it) to attack B antigens but not A antigens, since the sequences of the alleles on your ABO gene make the A-type antigens but not the B-type antigens. If you have one A allele and one B allele, then your red blood cells are covered with both A and B antigens, and you do not produce antibodies to fight either type of antigen. On the other hand, if you have two O alleles, you have no antigens on your red blood cells and therefore your immune system produces antibodies against both A-type antigens and B-type antigens. Once again, this is all determined by the sequences of the alleles for the ABO gene. Epigenetic processes determine how and when those alleles are read, but every red blood cell reads them and is covered by the antigens that their sequences code for. I have linked to you the details of the sequences of each allele and how they have been positively identified as determining blood type. You have simply ignored that.

          Once again, then, blood type has nothing to do with epigenetics. The sequence of both alleles determines the antigens on the red blood cells. Same with sickle-cell anemia. The sequence of the hemoglobin gene determines the hemoglobin in the red blood cell, which determines the shape. If you have one allele with the sickle-cell hemoglobin gene, half of your cells are sickle-shaped. If you have two alleles with the sickle-cell hemoglobin gene, all your cells are sickle. This has nothing to do with epigenetics.

          Please read the article that I have been trying to get you to read. It will probably clear up a lot of your confusion. I really don’t have time to educate you if you are unwilling to learn.

  3. John D says:

    I love this. I think men like Lamarck and Pierre-Paul Grassé would have loved to live to see these discoveries. My pedestrian theory is that there is “micro information” situated at a level which we are totally unfamiliar with. Similar to discreet packets. This differs from corporeal information.. it’s less tangible. You can literally feel it when someone throws a piece of wadded up paper at you and hits the back of the head. But you can also intuitively feel it when someone is thinking of doing the same and has taken some time staring at you with the thought… you can feel the eyes and the intention.

    In a similar way I think micro information is translated perhaps not along nervous systems but in overlapping energy fields. That every cell contains a full copy of DNA is interesting. That seems like a lot of information to carry around. Every micro program running in a computers OS does not contain a copy of the entire OS. Wonder if that extra information helps in some way.

    It seems, by what you have written above, that epigentics mitigates life by switching genes off and on when necessary. I wouldn’t be surprised if we find an underlying internal arbiter in the mutation selection process as well. The biggest failure of Darwinism is the negligence (of very intelligent people) to realize that external selection is nowhere near powerful enough to account for adaptation.

  4. Victor Ferreira da Silva says:

    Always nice to learn more about epigenetics! The more we discovery, the more we know that the idea that we are just genes is no sense!

    God Enlighten you all!

  5. Romance De says:

    This is fascinating stuff. It seems the more we learn, the more we find we don’t know. What I see here is further depth to the level of complexity of the genetic system and possibly some answers to the specialization of cells in complex organisms, especially in the early development of the organism.
    Am I to understand that these epigenetic mechanisms do not alter DNA sequences, but somehow can pass additional information from parent to child? Is it in the mDNA or somewhere else? So we know that mDNA has some kind of change over time. How does this affect the argumentation regarding evolution, particularly with speciation within a genome versus genetic drift of populations into new genomes?

    1. Jay Wile says:

      You are correct. Epigenetic mechanisms don’t change the DNA sequences. This is why the “power” of epigenetics is limited. DNA sequences exert the main influence on traits. Identical twins have identical DNA but are not identical. Their similarities are because of their identical DNA sequences. Their differences are because of epigenetics. The fact that identical twins are nearly identical shows the epigenetics has a limited effect on the organism.

      Yes, some epigenetic changes can be inherited. It’s not clear how many. There are lots of epigenetic changes that we know are not inherited. For example, lactose-intolerant parents will not have a lactose-intolerant baby. So the epigenetic change that causes lactose intolerance is not inherited. Also, in studies that have been done so far, if the stimulus goes away, the inheritance goes away in a few generations. In the mouse experiment I discussed, for example, the offspring inherited the fear epigenetically. If each generation was exposed to the fear-inducing smell a few times, it would continue to be inherited. However, if you stopped exposing the new generations to the fear-inducing smell, the fear would disappear in a few generations.

      Mitochondrial DNA (mDNA) is a small set of DNA in the mitochondria of the cells. It is not what controls most traits. Nuclear DNA (the DNA in the nucleus) contains the sequences that affect most of our traits. That’s what’s being discussed here. Also, the current view of biologists is that you only get mitochondrial DNA from your mother. That view, however, is beginning to change, at least in some cases. Mitochondrial DNA does change over time, because mutations do happen in it as well.

      The main thing epigenetic inheritance does to evolution is remove some level of randomness from it. In classical New-Darwinian theory, random mutations drive the changes that produce evolution. However, epigenetics has shown that this is not always the case. Sometimes, epigenetic changes caused by the environment drive the changes we see in organisms. The blind cave fish discussed in the article, for example, became blind because of epigenetic changes caused by the environment, not because of random DNA mutations.

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