Origins codes for DNA: Argument for design?

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November 13, 2015

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Here’s the abstract:

To unveil the still-elusive nature of metazoan replication origins, we identified them genome-wide and at unprecedented high-resolution in mouse ES cells. This allowed initiation sites (IS) and initiation zones (IZ) to be differentiated. We then characterized their genetic signatures and organization and integrated these data with 43 chromatin marks and factors. Our results reveal that replication origins can be grouped into three main classes with distinct organization, chromatin environment, and sequence motifs. Class 1 contains relatively isolated, low-efficiency origins that are poor in epigenetic marks and are enriched in an asymmetric AC repeat at the initiation site. Late origins are mainly found in this class. Class 2 origins are particularly rich in enhancer elements. Class 3 origins are the most efficient and are associated with open chromatin and polycomb protein-enriched regions. The presence of Origin G-rich Repeated elements (OGRE) potentially forming G-quadruplexes (G4) was confirmed at most origins. These coincide with nucleosome-depleted regions located upstream of the initiation sites, which are associated with a labile nucleosome containing H3K64ac. These data demonstrate that specific chromatin landscapes and combinations of specific signatures regulate origin localization. They explain the frequently observed links between DNA replication and transcription. They also emphasize the plasticity of metazoan replication origins and suggest that in multicellular eukaryotes, the combination of distinct genetic features and chromatin configurations act in synergy to define and adapt the origin profile. (paywall) – Christelle Cayrou, Benoit Ballester, Isabelle Peiffer, Romain Fenouil, Philippe Coulombe, Jean-Christophe Andrau, Jacques van Helden & Marcel Méchali.Genome Research, 11 November 2015.

These researchers’ findings make the genome sound like a committee, but without the usual duds, drones, and discards from more productive work groups that most human committees feature.

Thoughts?

Comments

Larry Moran:
We’ve known about origins of replication for almost 50 years.
What does that mean, Larry? Does it mean we knew it had an origin because we don't know how it originated, even to this very day. Also can you link to this alleged evolutionary theory so we can all see what it actually says so we can all see what actually challenges it? One more thing- you still have no idea what determines an organism's final form. Your reference to Venter proves that you don't have a clue.Virgil Cain_{November 16, 2015
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Professor Moran, Would you mind answering the questions @23 & @24? Yes. I'm only going to engage people who ask honest questions and genuinely want to learn something or have a serious discussion. I'll ignore everyone else. That includes you. Still not sure about Box.Larry Moran_{November 16, 2015
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Professor Moran, Would you mind answering the questions @23 & @24? Thank you. Here's the link to post 23: https://uncommondescent.com/design-inference/origins-codes-for-dna-argument-for-design/#comment-588266Dionisio_{November 16, 2015
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gpuccio RE: posts #18, #25, #30 If one or both of the mentioned nonessential functional parts, subsystems or mechanisms (small TV screens and power outlet) get removed, would the airplane still be able to perform its main function - i.e. fly and transport people from a location to another? Are there equivalent situations in biology research?Dionisio_{November 16, 2015
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Box says,
Larry Moran seems to be in denial about the challenge for neo-darwinian (and neutral theory) evolution posed by epigenetics.
Really? Let's take methylation of DNA as one of the classic example of epigenetics. We've known about that for 40 years and I've been teaching it for almost as long. We know the enzymes and we know how they work. We know how the epigenetic marks are inherited. Epigenetics Restriction, Modification, and Epigenetics Not it's entirely possible that I could be wrong about epigenetics and it really does present a challenge for evolutionary theory. Maybe I just missed it sometime over the past four decades. However, quoting Stephen Meyer as your authority on this subject seems to violate some of the principles you adhere to; namely, demanding that your "expert" really is an expert.Larry Moran_{November 16, 2015
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Larry Moran, "Two large sections of the mouse genome were deleted..." Isn't this the study where some of the deleted DNA is highly conserved, yet they found no obvious deleterious effects to the mice. What would cause this DNA to be conserved? Is there some tool that unusually conserves DNA other than natural selection?bFast_{November 16, 2015
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2. I understand that fish in a closely related family have genomes that are twice the size of pufferfish. What happens when scientists remove the excess DNA from the genomes of some of these fish and breed them for a few generations? Has this experiment been attempted, and if so, were any deleterious effects observed in the population with pruned DNA? Just curious.
No, nobody has done those experiments and nobody is ever going to do them. The experiment is too difficult and expensive and there are better ways to determine if the excess DNA is junk or not.
3. I understand that similar experiments were performed in mice a few years ago. Casey Luskin has a report on it here: http://www.evolutionnews.org/2.....62001.html
Two large sections of the mouse genome were deleted in a small-scale attempt to see if any of the putative genes in those regions really were genes. The mice seemed to survive very well suggesting strongly that there not dozens of functional genes in those regions as some people were predicting.Larry Moran_{November 16, 2015
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Vincent Torley asks,
1. Do scientists have any idea yet why pufferfish have such small genomes, or why onions have such large ones? It strikes me that until we can answer these questions and make quantitative predictions about the size of an organism’s junk DNA, we can’t really be said to have a scientific theory of junk DNA.
No, we don't know why pufferfish have small genomes and we don't know why two closely related species of onion can have very different genome sizes. We don't have (or want) a scientific theory of junk DNA in the sense you imagine. We're talking about the history of life here and these are unique events. The very best we can do is to make sure that evolutionary theory isn't violated or refuted by the existence of species with lots of junk DNA in their genome. In other words, evolutionary theory has to be compatible with what we observe. The older version of evolutionary theory (Darwinism) was NOT compatible but the modern version that includes Neutral Theory, random genetic drift, and advanced population genetics IS compatible. The modern version of evolutionary theory would strongly suggest that species with large population sizes and rapid reproduction rates would not have much junk DNA in their genomes. I would also indicate that species with small populations and slow reproduction rates would probably have a junky genome. These are probabilities. That's how biology works. Within the range of probably outcomes there are always going to be species in the tails of the probability distribution. You can't predict which particular species will have a genome size of "x." Think of it this way. The laws and theories of physics are very robust and well-confirmed. Yet they cannot predict how many planets we will find around a given main sequence star. Surely you don't think that's a flaw in the theories, do you? Or try this. Our understanding of what causes cancer is getting quite sophisticated. But we'll never be able to predict whether a given person will get bladder cancer or not. The best we can do is assign probabilities. We won't throw out our understanding of cancer if the person dies of a heart attack when they are 110 years old or if they die of leukemia when they are a child. You are asking for the impossible when you demand a theory that makes "quantitative predictions about the size of an organism’s junk DNA." I'm surprised you don't know this since you are an intelligent design proponent. Or am I missing something? Does ID make such quantitative predictions about junk DNA?Larry Moran_{November 16, 2015
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Hi Professor Moran, Thank you for your response. You wrote:
Why couldn’t our genome be one-tenth the size it is now in which case there would only be 10 mutations per generation? (The number of mutations per generation depends on the amount of DNA that’s being replicated.) This is what we see in pufferfish where a much smaller genome seems to work just fine. This is where the Onion Test becomes useful. Does your speculation pass the Onion Test?
I'd like to ask you a couple of questions. 1. Do scientists have any idea yet why pufferfish have such small genomes, or why onions have such large ones? It strikes me that until we can answer these questions and make quantitative predictions about the size of an organism's junk DNA, we can't really be said to have a scientific theory of junk DNA. 2. I understand that fish in a closely related family have genomes that are twice the size of pufferfish. What happens when scientists remove the excess DNA from the genomes of some of these fish and breed them for a few generations? Has this experiment been attempted, and if so, were any deleterious effects observed in the population with pruned DNA? Just curious. 3. I understand that similar experiments were performed in mice a few years ago. Casey Luskin has a report on it here: http://www.evolutionnews.org/2012/07/new_scientist_c062001.html Are there any comments you'd like to make on his piece? Thank you.vjtorley_{November 16, 2015
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gpuccio @25
I would add redundancy to the model [...] both attain the same result, in different ways.
Yes, agree. Good catch! Thank you for adding it. I missed that important part, which is seen in some well designed complex models, like in large passenger airplanes or computer servers for banking systems. BTW, sometimes I've noticed in some biology research papers, that their experiments intentionally altered something within the observed system, apparently expecting to see a particular behavior change, but were surprised to discover that the affected system still managed to 'survive' or get away with the introduced 'alteration'. Then sometimes the given conclusion referred to some kind of unexpected redundancy. Did I understand that correctly?Dionisio_{November 16, 2015
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Larry Moran @20
Then my daughter (Ph.D. in astrophysics) explains to me that they already new that;
Huh?! :)Dionisio_{November 16, 2015
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Larry Moran @20
I’m certain that you are an expert on something.
Well, sorry to disappoint you, but I'm not an expert on anything, not even on my own ignorance. BTW, I suffer an incurable natural human malady that makes me resistant to admit my ignorance.Dionisio_{November 16, 2015
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gpuccio @25
What is certainly “functional”, but not essential, and probably not even desirable, is the self-assurance of those who, considering themselves experts (and being indeed experts), think that they can impose their views by authority and maybe arrogance, instead than by honest and patient and respectful intellectual confrontation, however non essential it may be.
Eccellente!!! Mile grazie mio caro amico Dottore!Dionisio_{November 16, 2015
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Larry Moran seems to be in denial about the challenge for neo-darwinian (and neutral theory) evolution posed by epigenetics. On the Sandwalk blog, march 2014, Larry writes:
Larry Moran: We're only going to cover epigenetics for a few minutes in today's class because there aren't any serious arguments in favor of changing our view of evolution because of epigenetics. However, we are going to spend a lot more time learning that evo-devo is just as stupid because there are some seriously misled developmental biologists who think that discoveries in their field change how we should view evolution. :-)
That would be the day!
NEO-DARWINISM AND THE CHALLENGE OF EPIGENETIC INFORMATION These different sources of epigenetic information in embryonic cells pose an enormous challenge to the sufficiency of the neo-Darwinian mechanism. According to neo-Darwinism, new information, form, and structure arise from natural selection acting on random mutations arising at a very low level within the biological hierarchy—within the genetic text. Yet both body-plan formation during embryological development and major morphological innovation during the history of life depend upon a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. If DNA isn’t wholly responsible for the way an embryo develops—for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process. Genetic mutations are simply the wrong tool for the job at hand. Even in a best-case scenario—one that ignores the immense improbability of generating new genes by mutation and selection—mutations in DNA sequence would merely produce new genetic information. But building a new body plan requires more than just genetic information. It requires both genetic and epigenetic information—information by definition that is not stored in DNA and thus cannot be generated by mutations to the DNA. It follows that the mechanism of natural selection acting on random mutations in DNA cannot by itself generate novel body plans, such as those that first arose in the Cambrian explosion. [Stephen Meyer, ch.19, 'Darwin's Doubt']
It's pretty obvious why Larry is in denial mode: epigenetics spells disaster for his position.
Gpuccio #1: I don’t know what to say, but if I were a sincere neo darwinist, the emerging landscape of epigenetic control would probably encourage me to consider (intellectual) suicide. We have been saying many times, during the last few years, that the emerging complexity revealed by daily biological research is probably the strongest, ongoing argument for design. That is absolutely true. But I must say that the emerging functional complexity of the epigenetic landscape is really beyond all my most optimistic expectations!
Box_{November 16, 2015
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Dionisio @18: Yes, your example is fine. I would add redundancy to the model: maybe your wife looks at movies in the small video, and maybe you can look at movies on your laptop. You both attain the same result, in different ways. Larry Moran adds that "This blog would be an even better example". I can agree. Knowledge and intellectual confrontation are probably not essential. From some point of view. More essential from others. What is certainly "functional", but not essential, and probably not even desirable, is the self-assurance of those who, considering themselves experts (and being indeed experts), think that they can impose their views by authority and maybe arrogance, instead than by honest and patient and respectful intellectual confrontation, however non essential it may be.gpuccio_{November 16, 2015
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Larry Moran @20
Sharing “vast knowledge” with you is just going to be a waste of time.
Professor Moran, Apparently you started our chatting in this UD blog last October, didn't you? Can you explain what motivated you to write to me first? Here's a quick hint: https://uncommondescent.com/intelligent-design/are-some-of-our-opponents-in-the-grip-of-a-domineering-parasitical-ideology/#comment-587914 BTW, I assume you don't have to consult your academic colleagues in order to prepare for answering the above question, do you? :)Dionisio_{November 16, 2015
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Larry Moran @20
That’s an incorrect statement, verging on a lie.
Is yours a scientific statement?Dionisio_{November 16, 2015
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Larry Moran is old-school and still believes that organisms are little machines that are controlled by DNA and the environment. He tries to keep up and claims to have read ‘Darwin’s Doubt’, but he obviously skipped over the part on epigenetics. The days that DNA ran the show are long gone Larry ….
DNA helps direct protein synthesis. Parts of the DNA molecule also help to regulate the timing and expression of genetic information and the synthesis of various proteins within cells. Yet once proteins are synthesized, they must be arranged into higher-level systems of proteins and structures. Genes and proteins are made from simple building blocks—nucleotide bases and amino acids, respectively—arranged in specific ways. Similarly, distinctive cell types are made of, among other things, systems of specialized proteins. Organs are made of specialized arrangements of cell types and tissues. And body plans comprise specific arrangements of specialized organs. Yet the properties of individual proteins do not fully determine the organization of these higher-level structures and patterns.12 Other sources of information must help arrange individual proteins into systems of proteins, systems of proteins into distinctive cell types, cell types into tissues, and different tissues into organs. And different organs and tissues must be arranged to form body plans. The hierarchical layering or arrangement of different sources of information. Note that the information necessary to build the lower-level electronic components does not determine the arrangement of those components on the circuit board or the arrangement of the circuit board and the other parts necessary to make a computer. That requires additional informational inputs. Two analogies may help clarify the point. At a construction site, builders will make use of many materials: lumber, wires, nails, drywall, piping, and windows. Yet building materials do not determine the floor plan of the house or the arrangement of houses in a neighborhood. Similarly, electronic circuits are composed of many components, such as resistors, capacitors, and transistors. But such lower-level components do not determine their own arrangement in an integrated circuit (see Fig. 14.2). In a similar way, DNA does not by itself direct how individual proteins are assembled into these larger systems or structures—cell types, tissues, organs, and body plans—during animal development.13 Instead, the three-dimensional structure or spatial architecture of embryonic cells plays important roles in determining body-plan formation during embryogenesis. Developmental biologists have identified several sources of epigenetic information in these cells. CYTOSKELETAL ARRAYS Eukaryotic cells have internal skeletons to give them shape and stability. These “cytoskeletons” are made of several different kinds of filaments including those called the “microtubules.” The structure and location of the microtubules in the cytoskeleton influence the patterning and development of embryos. Microtubule “arrays” within embryonic cells help to distribute essential proteins used during development to specific locations in these cells. Once delivered, these proteins perform functions critical to development, but they can only do so if they are delivered to their correct locations with the help of preexisting, precisely structured microtubule or cytoskeletal arrays (see Fig. 14.3). Thus, the precise arrangement of microtubules in the cytoskeleton constitutes a form of critical structural information. These microtubule arrays are made of proteins called tubulin, which are gene products. Nevertheless, like bricks that can be used to assemble many different structures, the tubulin proteins in the cell’s microtubules are identical to one another. Thus, neither the tubulin subunits, nor the genes that produce them, account for the differences in the shape of the microtubule arrays that distinguish different kinds of embryos and developmental pathways. Instead, the structure of the microtubule array itself is, once again, determined by the location and arrangement of its subunits, not the properties of the subunits themselves. Jonathan Wells explains it this way: “What matters in [embryological] development is the shape and location of microtubule arrays, and the shape and location of a microtubule array is not determined by its units.”14 For this reason, as University of Colorado cell biologist Franklin Harold notes, it is impossible to predict the structure of the cytoskeleton of the cell from the characteristics of the protein constituents that form that structure.15 Another cell structure influences the arrangement of the microtubule arrays and thus the precise structures they form and the functions they perform. In an animal cell, that structure is called the centrosome (literally, “central body”), a microscopic organelle that sits next to the nucleus between cell divisions in an undividing cell. Emanating from the centrosome is the microtubule array that gives a cell its three-dimensional shape and provides internal tracks for the directed transport of organelles and essential molecules to and from the nucleus.16 During cell division the centrosome duplicates itself. The two centrosomes form the poles of the cell-division apparatus, and each daughter cell inherits one of the centrosomes; yet the centrosome contains no DNA.17 Though centrosomes are made of proteins—gene products—the centrosome structure is not determined by genes alone. MEMBRANE PATTERNS Another important source of epigenetic information resides in the two-dimensional patterns of proteins in cell membranes.18 When messenger RNAs are transcribed, their protein products must be transported to the proper locations in embryonic cells in order to function properly. Directed transport involves the cytoskeleton, but it also depends on spatially localized targets in the membrane that are in place before transport occurs. Developmental biologists have shown that these membrane patterns play a crucial role in the embryological development of fruit flies. Membrane Targets For example, early embryo development in the fruit fly Drosophila melanogaster requires the regulatory molecules Bicoid and Nanos (among others). The former is required for anterior (head) development, and the latter is required for posterior (tail) development.19 In the early stages of embryological development, nurse cells pump Bicoid and Nanos RNAs into the egg. (Nurse cells provide the cell that will become the egg—known as the oocyte—and the embryo with maternally encoded messenger RNAs and proteins.) Cytoskeletal arrays then transport these RNAs through the oocyte, where they become attached to specified targets on the inner surface of the egg.20 Once in their proper place—but only then—Bicoid and Nanos play critical roles in organizing the head-to-tail axis of the developing fruit fly. They do this by forming two gradients (or differential concentrations), one with Bicoid protein most concentrated at the anterior end and another with Nanos protein most concentrated at the posterior end. Insofar as both of these molecules are RNAs—that is, gene products—genetic information plays an important role in this process. Even so, the information contained in the bicoid and nanos genes does not by itself ensure the proper function of the RNAs and proteins for which the genes code. Instead, preexisting membrane targets, already positioned on the inside surface of the egg cell, determine where these molecules will attach and how they will function. These membrane targets provide crucial information—spatial coordinates—for embryological development. Ion Channels and Electromagnetic Fields Membrane patterns can also provide epigenetic information by the precise arrangement of ion channels—openings in the cell wall through which charged electrical particles pass in both directions. For example, one type of channel uses a pump powered by the energy-rich molecule ATP to transport three sodium ions out of the cell for every two potassium ions that enter the cell. Since both ions have a charge of plus one (Na+, K+), the net difference sets up an electromagnetic field across the cell membrane.21 Experiments have shown that electromagnetic fields have “morphogenetic” effects—in other words, effects that influence the form of a developing organism. In particular, some experiments have shown that the targeted disturbance of these electric fields disrupts normal development in ways that suggest the fields are controlling morphogenesis.22 Artificially applied electric fields can induce and guide cell migration. There is also evidence that direct current can affect gene expression, meaning internally generated electric fields can provide spatial coordinates that guide embryogenesis.23 Although the ion channels that generate the fields consist of proteins that may be encoded by DNA (just as microtubules consist of subunits encoded by DNA), their pattern in the membrane is not. Thus, in addition to the information in DNA that encodes morphogenetic proteins, the spatial arrangement and distribution of these ion channels influences the development of the animal. The Sugar Code Biologists know of an additional source of epigenetic information stored in the arrangement of sugar molecules on the exterior surface of the cell membrane. Sugars can be attached to the lipid molecules that make up the membrane itself (in which case they are called “glycolipids”), or they can be attached to the proteins embedded in the membrane (in which case they are called “glycoproteins”). Since simple sugars can be combined in many more ways than amino acids, which make up proteins, the resulting cell surface patterns can be enormously complex. As biologist Ronald Schnaar explains, “Each [sugar] building block can assume several different positions. It is as if an A could serve as four different letters, depending on whether it was standing upright, turned upside down, or laid on either of its sides. In fact, seven simple sugars can be rearranged to form hundreds of thousands of unique words, most of which have no more than five letters.”24 These sequence-specific information-rich structures influence the arrangement of different cell types during embryological development. Thus, some cell biologists now refer to the arrangements of sugar molecules as the “sugar code” and compare these sequences to the digitally encoded information stored in DNA.25 As biochemist Hans-Joachim Gabius notes, sugars provide a system with “high-density coding” that is “essential to allow cells to communicate efficiently and swiftly through complex surface interactions.”26 According to Gabius, “These [sugar] molecules surpass amino acids and nucleotides by far in information-storing capacity.”27 So the precisely arranged sugar molecules on the surface of cells clearly represent another source of information independent of that stored in DNA base sequences. [Stephen Meyer, ch. 14, ‘Darwin’s Doubt’].
Box_{November 15, 2015
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Dionisio asks,
Regarding your second item (b) in your commentary, would the following example qualify as a case of a designed object component or feature that is functional but not essential?
This blog would be an even better example. :-)Larry Moran_{November 15, 2015
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Dionisio says,
Facing so many interesting research papers we feel like children in a gigantic toy store.
I understand the feeling. I feel the same way when I read papers about astrophysics. Then my daughter (Ph.D. in astrophysics) explains to me that they already new that; it's wrong; or it's just an incremental addition to what they already know. Those are pretty much my reactions when I read about "exciting" new discoveries in biochemistry, molecular biology, and evolution. It a rare day when I read something new that has to go into my textbook. Dionisio, I'm certain that you are an expert on something. When you read popular press reports about new and exciting discoveries in your field do you feel like a child in a candy store or do you recognize that the popular press exaggerates a little bit?
As researchers dig deeper into more accurate levels of details, they discover more purpose-driven specified functional prescriptive information being transmitted and interpreted within the biological systems.
That's an incorrect statement, verging on a lie. "Researchers" are NOT discovering "purpose-driven specified functional prescriptive information." Just the opposite. Researchers in general are still convinced that there's no evidence of purpose in biochemistry and molecular biology. What you may be seeing is propaganda from Intelligent Design Creationists who are interpreting the data according to their preconceptions of what it should be demonstrating. Lawyer Barry Arrington will explain to you why their logic is faulty and their assumptions are incorrect. BTW, I can see now that you probably weren't telling the truth when you implied earlier that you had an open mind and just wanted to learn about developmental biology. Here's what you said a few days ago ...
When science is discussed seriously, we all benefit. In this case, given the highly disproportionate knowledge difference between a science professor and a nobody like me, the biggest beneficiary is the ignorant who can learn much from the friendly exchange of information, which is mostly a one-way flow. Again, thank you for your willingness to share your vast knowledge with me and other interested readers.
Here's what you said today.
Complex complexity. Indeed! The more we know, the more we have to learn. Unending Revelation of the Ultimate Reality.
Your mind is already made up. Sharing "vast knowledge" with you is just going to be a waste of time.Larry Moran_{November 15, 2015
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@10 Larry Moran "He and I disagree on a number of things. We’ve been arguing about them for almost twenty years. He continues to comment on Sandwalk from time to time. I’ve been to his house in Oxford to discuss our differences over molecular evolution. " Now I heard a rumor that I would like Professor Moran to confirm or deny if possible. I heard this rumor that when you went to Dawkins house, that you asked him where your cup of tea was and that Dawkins said that he was waiting for the tea to be made by chance for you. I heard that you got your own back though and when it came to the roast dinner then you started throwing the roast potatoes from your plate and when Dawkins said to you, what the hell are you doing Larry? Then you said, Richard, I am just testing the hypothesis that selecting something for elimination from my plate is going to create something that never was on my plate. Did this happen Professor?Jack Jones_{November 15, 2015
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gpuccio @16 Regarding your second item (b) in your commentary, would the following example qualify as a case of a designed object component or feature that is functional but not essential? The small TV screens that are attached to the back of the seats in the economy class of some airplanes are not essential, but definitely have a function. My wife sometimes watches films during our long flights. However, I rarely look at those screens, because I usually just read offline a few PDF documents I download before the flight. Another thing I consider very handy is the power outlet located right between our two seats, which allows me to charge my tablet during long flights. Though functional, that power outlet is not essential. If any of those two things (or both) were broken or removed, we still could get to our destination, assuming all the essential parts were in place and well. BTW, not sure if this is 'off topic' for this current thread, but wanted to let you know that for some reason your name came to my mind when I saw this: http://www.sciencedirect.com/science/journal/00145793/589/20/supp/PADionisio_{November 15, 2015
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Vincent Torley says,
Well, if we’re talking about all noncoding DNA, then Professor Moran is of course correct. But if we’re talking about most DNA, that’s another story entirely:
Thanks. Let's put a stop to this stupid myth about scientists thinking that since only 2% of our genome encodes protein therefore all the noncoding DNA (98%) is junk. It started out as a misconception (perhaps) but now it's a lie to repeat it.
But then I had a look at Dr. Richard Sternberg’s posts on LINEs and SINEs (see here, here and here), and I have to say I thought Dr. Sternberg made a good case for these segments being the product of design.
What you have to keep in mind is that the vast majority of SINES and LINES contain mutations that make them unable to transpose. In most cases, the signals consist of little more than bits and pieces of sequences that use to be intact SINCE and LINES. The total number of functional transposons in the genome accounts for less than 1%. About 50% of the genome consists of defective bits of transposons. That doesn't look like design to me. It looks like pseudogenes. I count the functional transposons as part of the functional fraction of the genome. Furthermore, it doesn't make sense to postulate that all the defective transposon fragments have secondarily acquired a function. There's suggestive evidence that a few of them might have a new function but even in order to arrive at a "few" you have to add together results from a dozen different species. Also, when you are thinking about this issue, remember that every newborn baby has about 100 new mutations. If most of our genome were functional then a huge number of these mutations are going to be detrimental and our species could not survive. It follows that most mutations have to be neutral which means that most of our genome has to nonfunctional junk DNA. This is the genetic load argument for junk DNA first advanced in the late 1960s.
Professor Moran, are you aware of any evidence that the genomes of organisms living 10 million, 100 million or 500 million years ago were smaller on average than they were today?
We talked about this when Carl was in Toronto last December preparing this article. Junk DNA comments in the New York Times Magazine I don't agree with Carl. I don't think there's any evidence that the immediate ancestors of humans had smaller genomes. However, it seems reasonable that once you get back 500 million years or so it's very likely that our ancestors had smaller genomes.
What I’m suggesting is that junk DNA could itself be a design feature, and that the percentage of junk DNA should be no higher than it needs to be, to ensure the long-term survival of the species.
This doesn't make sense. Why couldn't our genome be one-tenth the size it is now in which case there would only be 10 mutations per generation? (The number of mutations per generation depends on the amount of DNA that's being replicated.) This is what we see in pufferfish where a much smaller genome seems to work just fine. This is where the Onion Test becomes useful. Does your speculation pass the Onion Test?Larry Moran_{November 15, 2015
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VJ: Just a few thoughts: a) Transposons are certainly a powerful tool for the remolding of the genomes in the course of natural history. Whether such remolding is a random functionless process, or a guided one which designs function, or just the occasional object of random "exaptation" leading to function by mere luck, remains to be decided, and could be one of the important fileds of confrontation between ID and neo darwinism (in any of its forms). b) Saying that "every piece of the genome is essential" is not the same as saying that every piece, or most, of the genome is functional. Function is not the same thing as essentiality. We learn from design in general, and from biology in particular, that many functions can be redundant, and that a good design is often associated to "escape routes", to alternative ways of doing the same essential thing. Epigenetics is a wonderful example of many different levels interacting in flexible ways to realize highly efficient control. Therefore, a lot of the genome could be functional without being essential, and so the human species, as well as other species, can probably avoid becoming extinct in less than a century.gpuccio_{November 15, 2015
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Professor Moran writes:
There was never a time when knowledgeable scientists thought that all noncoding DNA was junk.
Well, if we're talking about all noncoding DNA, then Professor Moran is of course correct. But if we're talking about most DNA, that's another story entirely:
[T. Ryan] Gregory believes that while some noncoding DNA is essential, most probably does nothing for us at all, and until recently, most biologists agreed with him. Surveying the genome with the best tools at their disposal, they believed that only a small portion of noncoding DNA showed any evidence of having any function. But in the past few years, the tide has shifted within the field... In 1964, the German biologist Friedrich Vogel did a rough calculation of how many genes a typical human must carry... If the human genome was made of nothing but genes, Vogel found, it would need to have an awful lot of them — 6.7 million genes by his estimate, a number that, when he published it in Nature, he admitted was “disturbingly high.” Vogel speculated that a lot of the genome was made up of essential noncoding DNA — possibly operating as something like switches, for example, to turn genes on and off. But other scientists recognized that even this idea couldn’t make sense mathematically. On average, each baby is born with roughly 100 new mutations. If every piece of the genome were essential, then many of those mutations would lead to significant birth defects, with the defects only multiplying over the course of generations; in less than a century, the species would become extinct. Faced with this paradox, Crick and other scientists developed a new vision of the genome during the 1970s. Instead of being overwhelmingly packed with coding DNA, the genome was made up mostly of noncoding DNA. And, what’s more, most of that noncoding DNA was junk — that is, pieces of DNA that do nothing for us. (Is Most of Our DNA Garbage? by Carl Zimmer, New York Times, March 5, 2015. Bolding mine - VJT.)
While Professor Moran is here, I have a few questions for him. I'm still making up my mind about what proportion of the human genome is functional. Recently, I watched Professor P.Z. Myers' 2011 talk on junk DNA and I thought he'd made a pretty convincing case (but see here fro another perspective), especially regarding LINEs and SINEs. But then I had a look at Dr. Richard Sternberg's posts on LINEs and SINEs (see here, here and here), and I have to say I thought Dr. Sternberg made a good case for these segments being the product of design. Surprisingly, despite the fact that his posts were written five years ago, I haven't seen a refutation from the "unguided evolution" camp, yet. Do you have any comments, Professor Moran? I've had another thought about Carl Zimmer's article. Zimmer writes:
Over millions of years, the human genome has spontaneously gotten bigger, swelling with useless copies of genes and new transposable elements. Our ancestors tolerated all that extra baggage because it wasn’t actually all that heavy. It didn’t make them inordinately sick. Copying all that extra DNA didn’t require them to draw off energy required for other tasks. They couldn’t add an infinite amount of junk to the genome, but they could accept an awful lot. To subtract junk, meanwhile, would require swarms of proteins to chop out every single dead gene or transposable element — without chopping out an essential gene. A genome evolving away its junk would lose the race to sloppier genomes, which left more resources for fighting diseases or having children.
Professor Moran, are you aware of any evidence that the genomes of organisms living 10 million, 100 million or 500 million years ago were smaller on average than they were today? Finally, here's a thought for ID theorists to ponder. Zimmer's article argues that if every piece of the genome were essential, then the human species would become extinct in less than a century. On that logic, there must be some critical percentage P of junk DNA in the human genome that would allow the human species to continue over very long periods of time (say, a million years). What I'm suggesting is that junk DNA could itself be a design feature, and that the percentage of junk DNA should be no higher than it needs to be, to ensure the long-term survival of the species. Thoughts?vjtorley_{November 15, 2015
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Larry Moran @8
We’ve known about origins of replication for almost 50 years. I worked on them a little bit when I was a graduate student in 1968.
Since then, some outstanding questions have been answered, but new important questions have been raised. That's why we look forward, with growing anticipation, to reading future research papers that might shed more light on the elaborate cellular and molecular information-processing choreographies orchestrated within the biological systems. This is a fascinating time to look at the very interesting data coming out of biological research, which is increasingly revealing a marvelous complexity that is turning more complex with every discovery. Just look at gpuccio, an experienced medical doctor, who reacts with such a contagious enthusiasm at the latest publications of new biological discoveries. Here's a recent example: https://uncommondescent.com/genomics/the-amazing-design-of-the-genome/#comment-588110 Facing so many interesting research papers we feel like children in a gigantic toy store. As researchers dig deeper into more accurate levels of details, they discover more purpose-driven specified functional prescriptive information being transmitted and interpreted within the biological systems. Complex complexity. Indeed! The more we know, the more we have to learn. Unending Revelation of the Ultimate Reality.Dionisio_{November 15, 2015
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Additional related papers referenced @1153-1160 here: https://uncommondescent.com/intelligent-design/mystery-at-the-heart-of-life/#comment-587959Dionisio_{November 15, 2015
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I’ve been to his house in Oxford to discuss our differences over molecular evolution. Did that come in a mug or a bottle?Mung_{November 14, 2015
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Granted then not a nimcompoop but not knowledgeable either.Andre_{November 14, 2015
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Andre asks, I take then that Richard Dawkins is not a knowledgeable scientist but quite possibly a nimcompoop? He's not a nimcompoop. He and I disagree on a number of things. We've been arguing about them for almost twenty years. He continues to comment on Sandwalk from time to time. I've been to his house in Oxford to discuss our differences over molecular evolution. We respect each other's position even though we each think the other person is wrong. Richard Dawkins Talks About the Human Genome Richard Dawkins' View of Random Genetic Drift Larry Moran_{November 14, 2015
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