T_aquaticus
(The Friendly Neighborhood Atheist)
61
I’m not playing that game. Either explain it or agree that the explanation doesn’t exist.
You are making the false assumption that transcription of non-functional DNA is harmful. It isn’t in the vast, vast majority of cases. These are often just one or a handful of transcripts that are quickly degraded.
Also, the Lynch and Marinov (2015) paper demonstrates that transcription of non-functional DNA will be below the level of selection in most animals and plants.
That has nothing to do with the transcription of non-functional DNA.
And they are???
Why can’t you copy and paste it? Why should I have to guess which parts you are referring to? You are the one making claims of what is in the paper, so it is up to you to quote it.
Throughout this thread, you have been responding to comments by defending and selling the paper. Which is fine, you are not obliged to yield anything. Bluntly, my own assessment is this be quantum woo, but what I think is of no consequence.
So far however, this work has been rejected by the Royal Society Open Science, PNAS Nexus, and Qeios, even though these journals solicit interdisciplinary explorations.
The point is that it is not me or anyone here you have to convince if the objective to to publish in a reputable journal. The real reason you are not getting past the first gate may well concern the rigor and coherence of your paper rather than anything thing to do with scope or availability of reviewers.
You don’t have to guess which parts because I told you exactly where it is.
Your citation of Lynch and Marinov (2015) overlooks more recent research that challenges the idea that random transcription of non-functional DNA is largely harmless. For example, a study by Long Qian and Edo Kussell (2016) found that non-functional protein-DNA binding can cause interference effects, disrupting vital molecular processes like transcription, gene regulation, replication, and mutational repair. Their findings suggest that genomes have evolved mechanisms to minimize weak, non-functional binding motifs to prevent these disruptions.
The study you refer to argues that evolutionary constraints have shaped genome-wide motif statistics to reduce weak binding, highlighting how genomes adapt to avoid potential detrimental effects of random interactions. This research suggests that non-functional binding may not be as benign as previously assumed, adding complexity to the understanding of non-functional DNA transcription:
That was not the point of referencing the study. Instead, it is to show how it is a highly precise finely tuned process that has to be this way or else the biochemical processes in the cell would grind to a halt.
Causal role definition of function and Ayala (2007) explains that random “mutations are unoriented with respect to adaptation; they occur independently of whether or not they are beneficial or harmful to the organisms”
Sure, that is still possible. For instance, we also had it peer-reviewed (informally) by three qualified experts and made major improvements off that feedback. We are waiting for two more reviews that will follow-up on whether those improvements and revisions are sufficient.
T_aquaticus
(The Friendly Neighborhood Atheist)
64
Those sections are made up of multiple paragraphs covering multiple topics. You need to specify the actual material in those sections that you are referring to.
Actually, they don’t run any assays that could possible show “interference effects”. All they were able to show is a lower number of DNA binding motifs than would be expected.
There is also the factor of sequence conservation within the transcripts. How is it that these transcripts can maintain function while mutating at a rate consistent with neutral drift?
This doesn’t prevent off target reactions. Anyone who has worked with proteins in any meaningful way will tell you that proteins can bind to a whole host of targets.
Which is a no go. That is enough reason to not publish the paper. The mere existence of a transcript is not evidence that it has function.
It is multiple paragraphs because it requires a detailed explanation to answer and address your objection, but it is only under one topic for each objection you make. Besides, if I start copying pasting these paragraphs from the paper, it may put things out of context and make it even more confusing.
I don’t know, but I asked ChatGPT and this is the answer it gave:
The factor of sequence conservation within transcripts is crucial to understanding their functional relevance. If these transcripts were truly non-functional, we wouldn’t expect them to display any significant sequence conservation. However, studies have shown that even regions assumed to be under neutral drift exhibit signs of selective pressure that preserve essential functional elements.
While some sequences may mutate at rates consistent with neutral drift, it’s possible that only certain critical portions of these transcripts are subject to strong selective constraints, allowing non-critical regions to accumulate mutations without losing overall function. This balance could explain how functional transcripts persist while still undergoing apparent neutral drift in less essential regions of the sequence.
Furthermore, it’s worth considering that conservation can extend beyond primary sequence to include structural or regulatory roles, which might be less visible in typical sequence-based conservation studies but still crucial for function.
Ok, but what is your point here?
It’s not about the mere existence of transcripts, but rather their necessity in biological processes, as I’ve already pointed out. The existence of a transcript is just one piece of evidence, and the functional relevance comes from its specific role in gene regulation, transcription, or other molecular processes.
Furthermore, the definition of “function” has evolved since the earlier criticisms of ENCODE. The ENCODE project no longer equates biochemical activity with function. The revised definition emphasizes that functional elements must produce reproducible and specific effects on biological processes or phenotypes. Biochemical activity alone is not enough to qualify as functionality, and this shift addresses previous concerns.
This new approach allows for a more refined understanding of genome function, acknowledging that not all biochemical signals indicate function, and instead focuses on elements that have verifiable impacts on biological systems.
T_aquaticus
(The Friendly Neighborhood Atheist)
66
Stopped reading there.
The point is that proteins can bind off target, even though they may need specific conformations in order to bind to a specific target 99.9% of the time.
The only evidence you have put forward for their function is their existence (i.e. the ENCODE study). You have not shown any assays which demonstrate actual function for the transcripts that cover ~70% of the human genome as discovered in the ENCODE study.
That’s the same definition. Being transcribed fits the “specific effects on biological processes” criteria.
If this is not the criteria you are using, then please point to the papers that actually look at the function of these transcripts. Mind you, not a miniscule handful, but the majority of them that supposedly cover ~70% of the human genome.
In that case, don’t expect me to copy and paste a bunch of excerpts from our article when you can just read it or copy and paste it yourself. What’s fair is fair.
Achieving absolutely zero non-specific binding is unlikely to be possible, as there will always be some degree of non-specific binding due to the random collision of molecules and the existence of weak interactions between them.
While non-specific binding is inevitable, biological systems have evolved to minimize its negative effects. Mechanisms like spatial compartmentalization and molecular proofreading help reduce the potential harm of non-specific interactions. These evolutionary safeguards ensure that cellular processes proceed efficiently, even with a background of non-specific interactions.
It’s not a big leap to propose that the competitive endogenous RNA (ceRNA) hypothesis provides a comprehensive model for pseudogene function. This hypothesis not only identifies potential functions for individual members of this so-called “junk” DNA class but also offers a broader framework that can explain the functional roles of many, if not all, members—whether directly in protein synthesis or indirectly in gene regulation.
As Mattick and Dinger have pointed out, noncoding RNAs, when tested, frequently demonstrate biological function across various developmental and disease contexts:
"Usually show evidence of biological function in different developmental and disease contexts, with, by our estimate, hundreds of validated cases already published and many more en route. This subset is large enough to draw broader conclusions about the likely functionality of the rest.
This evidence aligns with the specific and dynamic epigenetic modifications across most of the genome and supports the ENCODE finding that 80% of the genome exhibits biochemical indices of function (Dunham et al., 2012). If this is accurate, it challenges the long-standing protein-centric view of gene structure and regulation in human development, which may explain some of the resistance in certain scientific circles."
Additionally, Professor Alistair Forrest and his research team at the Harry Perkins Institute of Medical Research have identified numerous functional examples within noncoding regions:
“There is strong debate in the scientific community on whether the thousands of long non-coding RNAs generated from our genomes are functional or merely byproducts of noisy transcriptional machinery. Our findings provide compelling evidence that the majority of these long non-coding RNAs appear to be functional, with nearly 2,000 of them potentially involved in diseases and other genetic traits.”
Thus, given the growing body of evidence, it is far more likely that these regions of the genome have important functional roles, even though alternative explanations exist. The evidence supporting widespread functionality in noncoding regions makes this the most probable conclusion.
Are you still referring to the casual role definition of function here?
T_aquaticus
(The Friendly Neighborhood Atheist)
68
Having ChatGP write your posts is an abdication of discussion. Refusing to read posts written by an AI is not the same as asking for direct quotes from a paper (presumably) written by humans.
The background still exists.
Again, this is the type of activity that we would expect from the transcription of non-functional DNA. They will, by chance, have complementary sequence that would bind miRNA. What you would need to show, at a minimum, is sequence conservation of these complementary sequences and some type of actual function.
How many have shown evidence of function?
Let’s look at long non-coding RNA (lncRNA). They are 1kb to 10kb in length, and there are about 30,000 of them. Using the high end of the size spectrum, that is at most 300 million base pairs which is just 10% of genome. This is using the MOST generous size estimate and assuming every single one has function. A more realistic number is probably 0.1% of the genome being made up of actual functional lncRNA’s.
What percent of the genome is made up of these functional lncRNA’s? Is it 80%? Or is it closer to 1 or 0.1%?
Yes, the claim that the mere existence of a transcript means it is functional.
The authors also acknowledge the assistance of ChatGPT, an AI language model developed by OpenAI, for editing this manuscript and describing how all the predictions could be tested through specific experimental designs, statistical analyses, and criteria for falsification
1 Like
T_aquaticus
(The Friendly Neighborhood Atheist)
70
Yet another reason why the paper should be rejected.
You’re asking for more than just direct quotes—I’ve provided the sources and specific locations where you can easily find and verify the information yourself. Instead of discussing the content based on mutual research, you expect me to copy and paste large sections of text repeatedly. If you’re unwilling to engage in the effort of reading or sourcing the material yourself, it’s unreasonable to expect me to do all the work in our discussion. Effective discourse is a two-way street, and mutual effort is essential for a productive exchange.
I acknowledge that there is still much we don’t know about so-called “junk” DNA, and it’s true that many genetic elements, such as pseudogenes and ERVs, have not had specific functions attributed to them yet. However, recent research trends point to far more functionality in non-coding regions of the genome than was previously anticipated. For instance, a 2023 academic book on RNA suggests that “the genomes of humans and other complex organisms are not full of junk but rather are highly compact information suites, largely devoted to the specification of regulatory RNAs.” These RNAs are increasingly recognized as crucial in driving differentiation, brain function, and even transgenerational inheritance, challenging long-held dogmas in genetic programming.
C. Luskin, Comparing contemporary evangelical models regarding human origins. Religions 14, 748 (2023).
As for the binding of transcription factors to DNA, it is reasonable, though not certain, to infer that these binding sites play a role in regulating gene expression, given the vast amount of evidence supporting this relationship. While sequence conservation could provide additional evidence of function, conservation alone isn’t always the determining factor. Functionality can manifest through regulatory roles, RNA dynamics, or context-specific processes, which may not be easily captured by sequence conservation alone.
The conclusion drawn by ENCODE and other studies—that sequences binding transcription factors are functional—may still involve uncertainty, but it’s grounded in a solid understanding of how gene regulation operates. Confirmatory experiments, of course, remain necessary to reduce this uncertainty, but the inductive reasoning applied here is reasonable and aligns with broader patterns observed in molecular biology.
Hypothesis: @RTBsupporter no longer has access to an on-line copy of the paper, or has been banned from posting excerpts from it.
Test: See if @RTBsupporter ever posts any text cut-and-pasted from the paper, or just produces endless dubious excuses for not doing so.
Results: Coming soon…
2 Likes
T_aquaticus
(The Friendly Neighborhood Atheist)
73
Just asking for quotes.
You could also discuss it in your own words if you don’t want to quote it.
What percentage of the genome are made up of regulatory RNA’s according to this study, and how did they determine function?
What evidence???
You are trying to claim that around 80% of the genome is functional. What you need to explain is why 70% of the functional DNA in the human genome is accumulating mutations at a rate consistent with neutral drift. That doesn’t make any sense, especially given the other ID/Creationist arguments surrounding the rarity of function in sequence space. Why isn’t there any evidence of selection against deleterious mutations in this DNA?
What understanding is that?
What inductive reasoning? That the mere existence of a DNA binding motif is evidence that it is functional? That doesn’t sound like good reasoning to me.
Please @RTBsupporter quote your own paper. In all of the space in this thread that you have taken refusing to do so, you could have easily cited half of your paper by now.
Consider this post an informal warning about this thread being shut down due to your antics.
This strikes me as something a grad student defending a thesis might say when he doesn’t even remember his own paper well enough to immediately quote the pertinent material. Defense of a position does not rely on getting the critic to do the work, it relies on the defender knowing the material well enough to cite the relevant portion in a response.
This makes me wonder if you even are suitably enough familiar with the paper to be advocating for it.
Ditto that! I’ve caught ChatGPT several times inventing references and making plainly false statements to expect reliability.
You’re the one doing a defense; it’s up to you to demonstrate that you know the material. When a professor asked about something in my thesis during my defense, it was up to me to both reference and cite where I had addressed that, or to admit a weakness in my work.
I’m happy to summarize the core concepts from the article here. However, for the depth and nuance that may answer your specific questions, I would recommend reading the sections I previously mentioned. Alternatively, I’d appreciate an endorsement on the preprint server if you want me to put the extra effort in our discussion and give into your demands of copying and pasting large excerpts repeatedly. You can learn more about endorsements here: Endorse a Preprint - OSF Support
We’re using the causal role definition of function and Ayala’s definition of randomness, where mutations are “unoriented with respect to adaptation” and occur without regard to benefit or harm. Now, I’ll explain why we consider mutations to be “guided” in terms of external teleology, not internal teleology.
Roger Penrose’s Orch-OR theory proposes that consciousness arises from wave function collapse in microtubules, a unique process enabling non-computable tasks like contemplation and judgment. Quantum particles exist in superpositions, described by wave functions, until observed; this observation causes a collapse into a specific reality, a process possibly linked to consciousness.
Aerts and Arguëlles (2022) demonstrated that quantum theory could model cognitive processes such as decision-making, and recent studies show neural networks can exhibit quantum-like behavior. Some researchers suggest that, at a fundamental level, physical reality might resemble a neural network, with evidence linking quantum effects to bird species’ magnetic sensing. Penrose posits that consciousness results from orchestrated quantum processing in microtubules, leading to a unified experience.
Structuralists have also theorized that microtubules represent molecular forms emerging from self-organization, aligning with Richard Owen’s view of a divinely influenced archetype. Patel suggests the genetic code’s structure mirrors quantum algorithms, allowing efficient, error-tolerant protein synthesis. This may imply that natural selection capitalized on DNA’s quantum properties for precise replication.
Further research reveals biological systems, like electron transfer in energy production, exhibit quantum tunneling similar to engineered devices, showing optimization beyond classical theory. These insights bridge quantum mechanics and biological processes, underscoring a sophisticated natural design in biological functions.
Owen’s framework suggests that biological diversity derives from a universal archetype, an underlying form expressed across generations. This archetype theory, which Owen termed ‘metagenesis,’ implies that distinct organisms emerge from a shared structural base, adapting in ways that produce varying forms. This model contrasts with Darwin’s nested hierarchy view, where shared traits suggest common descent through evolutionary branches.
Owen attributed such nested patterns to structural laws, influenced by polarizing forces and adaptive needs similar to the law of entropy, which organizes matter by dispersing energy. Owen’s universal archetype applies to both living and non-living systems, suggesting a divine influence or natural order guiding structural adaptations. This order fosters variations that appear distinct yet adhere to an underlying blueprint, illustrating diversity within a unifying pattern. This hierarchical structure is shaped by environmental adaptation and intrinsic design principles, not solely by lineage.
In biology, establishing causal roles for structures or processes involves independent testing, often through experimental or observational studies. Owen’s extended theory posits that if entities exhibit necessary causal roles—meaning they exist due to inherent necessity—then this could reflect an underlying universal design. ENCODE’s research highlights functional predictions within noncoding genome regions previously labeled as ‘junk DNA.’ This presents a counterpoint to Darwinian evolution, which often interprets these as evolutionary remnants, while Owen’s view suggests a structural necessity in these regions.
Some evolutionary elements, like non-functional ERVs and pseudogenes, may initially seem to contradict intelligent design. However, they raise questions about evolutionary remnants’ role in a divinely influenced design, particularly when considering noncoding regions’ confirmed roles. This nuanced approach suggests that the genome’s architecture may be optimized for complex functions, highlighting a sophisticated regulatory system.
According to a 2023 book on RNA by John Mattick, a substantial part of the genome, especially in complex organisms like humans, comprises non-coding regions that are dense with regulatory RNAs, playing crucial roles in cellular differentiation, brain function, and heritable traits. However, the specific percentages does not seem to be universally confirmed according to them.
I guess I am referring back to ENCODE’S follow up paper in 2020…“as saying that 80 % of the genome is engaging in relevant biochemical activities that are very likely to have causal roles in phenomena deemed relevant to biomedical research.”
Germain, Pierre-Luc; Ratti, Emanuele; Boem, Federico (November 2014). “Junk or Functional DNA? ENCODE and the Function Controversy”. Biology & Philosophy . 29 (6): 807–831. doi:10.1007/s10539-014-9441
No, that is what ENCODE claims. We just claimed that majority of it is functional, and their results confirm that, at the moment.
For what I am able to understand, ENCODE’s findings on transcription factor-binding sites are apparently based on gene regulation principles, where transcription factors control gene activity by binding to DNA. These sites suggest regulatory roles even in non-coding DNA, potentially influencing cellular functions. While such binding generally implies functionality, it doesn’t confirm all these sites are essential, hence the lingering uncertainty.
1 Like
T_aquaticus
(The Friendly Neighborhood Atheist)
79
I would have to be convinced there is good science in the paper before I would endorse it. You came to this forum asking for reviewers and discussion, and that will necessarily require reference to the paper.
Which is nonsense.
You would have to demonstrate that observations require a consciousness. This is what Penrose’s Orch-OR theory has failed to support. We can see a whole lot of absorbance and emission spectra coming from cosmological bodies, and that requires a collapse of wavefunctions. Are you saying that a consciousness is guiding each and every photon in these cosmological bodies?
You have the cart in front of the horse. Just because quantum processes may be involved in consciousness does not mean all quantum processes are produced by consciousness.
How does it contrast? What predictions does Owen’s model make that differ from the expected nested hierarchy derived from evolutionary processes? If the two models make identical predictions then the theory of evolution wins out because it is based on observable and testable processes.
You should also explain why a universal archetype would produce a nested hierarchy? For example, why would this model prevent species from having combinations of mammal and bird features?
It’s still nonsense. Just existing does not make something functional.
Many of us are well aware of Mattick’s claims. The problem is that he has not supported these claims with evidence. We are still stuck with the observation that 90% of the genome is accumulating mutations at a rate consistent with neutral drift. It makes no sense that no deleterious mutations can occur in a functional piece of DNA.
ENCODE does not confirm that a large portion of the human genome has function.
Some transcription factor binding sites regulate the expression of functional DNA, not all of them.
What is good science to you then? I would need some sort of criteria you have in mind so I can adequately make the case.
Yes, but not necessarily demands of copying and pasting large excerpts repeatedly. This is going beyond what I expected and thus I would expect more from you in return.
According to your opinion and theory, Yes. But, this is not the case for us, at least under these circumstances.
I agree but this does not apply to Owen’s theory because there are fundamental differences between both theories. For instance, While Penrose’s Orch-OR model suggests consciousness arises from spontaneous wave function collapse influenced by gravity at the Planck scale, our perspective differs in attributing this collapse to interactions between non-local consciousness and quantum-level gravitational effects, with quantum fluctuations in dark energy playing a key role. Unlike Penrose’s reliance on Conformal Cyclic Cosmology for the universe’s origin, our approach aligns with eternal inflation, positing gravity as an intrinsic component of the wave function itself. I think these differences allow Owen’s theory to overcome most of those failures and objections you suggested.
Yes
Aerts and Arguëlles’ study specifically shows how quantum models can represent decision-making but does not claim that consciousness drives all quantum events.
We recommend further phylogenomic analysis to assess whether specific taxonomic groups warrant separate classification and if fossil record gaps between them are genuine, challenging aspects of evolutionary theory. Unlike the common descent model, which broadly categorizes taxa (e.g., reptiles and mammals), our approach suggests that phylogenomic data could clarify whether anatomical and molecular classifications align better with a common design. Testing this hypothesis involves comparing anatomical trees with molecular similarities across taxa to reveal if these patterns reflect complex relationships beyond linear evolutionary descent. So far, observations support our view:
C. Parins-Fukuchi, G.W. Stull, S.A. Smith, Phylogenomic conflict coincides with rapid morphological innovation. Proc. Natl Acad. Sci. U. S. A. 118 (2021).
In software engineering, principles like easier maintenance, code reuse, and scalability are closely tied to the concept of nested hierarchy. While strict adherence to hierarchies may not always be suitable, engineers have recognized their utility in designing complex systems more efficiently and faster.
You keep straw manning our argument. Again, there is a difference between existing and existing by necessity. The latter is what we are arguing in the article.
According to your definition of function, I agree.