Given that Ron’s post was 8 months, and a couple of dozen posts, ago and your “answer” is only tenuously related to it, I see no reason not to blame you.
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That would predict the absence of a nested hierarchy among orders, as well as the absence of large numbers of functional genes in the common ancestors of two orders. For example, if bats and rats evolved separately from slime molds (not really slime molds, but some primitive stem-metazoan), we would not expect them both to have four Hox clusters, each with the same gene complement. Only two rounds of gene duplication early in the vertebrate lineage would produce such a thing, and a primitive metazoan would have no use for four Hox clusters.
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Bovine faeces.
That study doesn’t even mention marine bacteria, horizontal gene transfer, subpopulations or ecological niches.
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That’s exactly how it’s constructed.
How did they determine function?
Why isn’t it probable?
WHY???
Nothing here supports your claim. Let’s say half of the transcription factor proteins bind to non-specific sites. That still leaves half to bind to far fewer functional binding sites. They work just fine.
Yes, it does. Word salad is useless and invalid.
Nowhere do they claim that mutations are guided to specific bases in response to specific environmental stimuli.
The few violations that we see are extremely minor and what we would expect from common ancestry.
The fossil record is not a valid measure of what species existed in the past. Fossilization is a highly biased process, as is the search for fossils.
You guys have yet to support your argument that it isn’t illusory.
All of which is a naturally occurring process.
There is no reason why this would produce a nested hierarchy.
Why would this produce a nested hierarchy???
Just as we would expect from common ancestry.
Why would this produce a nested hierarchy???
WHY???
What relevance does this have???
Again, they didn’t simply identify a few examples of function in particular members of a junk DNA category and then conclude the whole class must be functional. Instead, they identified, one by one, members of a sequence elements group that displayed function.
To determine the function of these elements, ENCODE used a combination of experimental and computational approaches, including:
-
Chromatin Immunoprecipitation sequencing (ChIP-seq): This method involves the use of antibodies to pull down specific DNA-binding proteins, such as transcription factors or histones, along with the DNA fragments they are bound to. These fragments are then sequenced and mapped back to the genome to identify regions of the genome that are bound by the protein of interest, indicating potential regulatory regions.
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RNA sequencing (RNA-seq): This method involves sequencing RNA transcripts in a cell or tissue sample, which can help identify functional elements such as protein-coding genes, non-coding RNA genes, and splice sites.
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DNA methylation profiling: This method involves measuring the levels of DNA methylation at specific sites in the genome, which can help identify regulatory regions and other functional elements.
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Computational analysis: ENCODE researchers also used computational methods to identify functional elements, such as identifying conserved sequences across species, predicting the effects of genetic variations on gene expression, and using machine learning algorithms to predict the function of non-coding DNA sequences.
Overall, ENCODE used a multi-pronged approach to identify and characterize functional elements in the human genome, and their findings have significantly expanded our understanding of the complexity and diversity of genomic regulation.
Because ENCODE’s conclusion is more probable. For instance, a vast body of data demonstrates that transcription factors bind to specific DNA sequences that regulate gene expression. Even though another explanation for why these transcription factors bind to DNA may exist as you pointed out, future experiments can reduce this uncertainty.
The key point is this: There is nothing wrong with the reasoning the ENCODE Project employed to assign function to sequences in the human genome because they were making use of induction (as do all scientists), not deduction.
Fuz Rana suggested in relation to this that…
“Transcribing 60 percent of the genome when most of the transcripts serve no useful function would routinely waste a significant amount of the organism’s energy and material stores. If such an inefficient practice existed, surely natural selection would eliminate it and streamline transcription to produce transcripts that contribute to the organism’s fitness.”
So the point of this quote is to show that Transcription binding could NOT logically be a random process as I think you might have been suggesting. Instead, 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.
I can condense it to just " universal self-collapsing genetic code" if this is the main issue.
This is not natural vs. supernatural processes, but it is unguided vs. guided natural processes. All we see is guided natural processes in nature based on the fine-tuning constants. For instance, quantum tunneling needs to be extremely precise for hemoglobin to transport the right amount of oxygen to the cells of all vertebrate and most invertebrate species.
So if the conscious observer chooses to measure the momentum of a particle with precision, the observer discovers that the position of the particle is now known only approximately ± half a mile. However, according to the Heisenberg principle, the more precisely the position of some particle is determined, the less precisely its momentum can be predicted from initial conditions, and vice versa. If the uncertainty in the position becomes much greater or smaller than half a mile, hemoglobin will not function as it does, rendering advanced life impossible.
This means that, despite the Heisenberg principle being a random process, the uncertainty in the Heisenberg uncertainty principle must be fine-tuned. This shows how the right fine-tuning values were carefully chosen to allow advanced life to exist from the beginning leading up to the present.
You and @Mercer are getting confused between prediction and hypothesis. “Guided mutations”, which imply a level of intention or directionality by a personal agent, is the hypothesis that is already supported by the fine-tuning constants.
“Non-random mutations” is the confirmed predictions that flows out of the guided mutations hypothesis that suggests a personal agent is involved in the process.
Well, I gave you the studies showing that it is definitely not minor.
This is because we don’t have the burden of proof. Owen’s saltational theory preceded Darwin’s claim about seeing gradualism in the fossil record. So the onus is not on us to refute your additional claim. You need to support it because you were the one that made it.
Not true. For instance, phylogenetic relies on similar features to draw or reconstruct phylogenetic trees. These features can be morphological, molecular, or behavioral traits that are shared among different organisms, but the most commonly used features are morphological and molecular traits that are shared among different organisms.
Observations show that viruses were not only the probable precursors of the first cells but also helped shape and build the genomes of all species through HGT.
Because regulatory networks are complex and hierarchical in nature, with individual transcription factors regulating the expression of multiple downstream genes, which in turn can regulate the expression of other genes.
When a new regulatory element is acquired through HGT, it is integrated into the existing regulatory network of the recipient organism, and its downstream targets become part of the regulatory network as well. Over time, the regulatory network can become more complex and hierarchical as additional regulatory elements are acquired.
As a result, even in cases of HRT, the regulatory networks of different organisms can still exhibit a nested hierarchy, with more closely related organisms sharing more similarities in their regulatory networks than distantly related organisms. This hierarchical structure arises because regulatory networks are constrained by the underlying biology of the organism, and changes to the regulatory network must be integrated into the existing network.
In summary, while HRT can complicate the formation of a clear nested hierarchy based solely on gene sequences, the hierarchical nature of regulatory networks can still result in a nested hierarchy of evolutionary relationships, even in cases of HGT.
Because closely related species may have similar physical or behavioral traits that allow them to exploit similar resources, leading to competition between them. In contrast, distantly related species may have different traits that enable them to use different resources, reducing competition and promoting coexistence.
No, if bats and rats evolved separately from a primitive stem-metazoan, we would not expect to see the absence of large numbers of functional genes in the common ancestors of these two orders. This is because the common ancestor of two groups of organisms would have possessed a full complement of genes that were present in the ancestral population.
The loss of genes can occur over time due to various evolutionary processes, such as genetic drift, gene duplication followed by subfunctionalization or neofunctionalization, or gene loss due to lack of selection pressure or redundancy. However, these processes typically occur after the divergence of lineages, and the loss of genes in one lineage is not necessarily mirrored by the loss of the same genes in another lineage.
Therefore, if bats and rats evolved separately, we would expect the common ancestors of these two orders to possess a full complement of genes, including functional genes that are absent in one or both of the modern lineages.
Furthermore, if bats and rats evolved separately from primitive stem-metazoans, they would still share many characteristics with other organisms that evolved from those same ancestors. For example, both bats and rats are mammals, and they share many common traits with other mammals, such as hair, mammary glands, and a four-chambered heart. These shared traits would place them within the nested hierarchy of mammals.
In addition, even if bats and rats evolved separately, they may have still evolved similar adaptations due to similar environmental pressures or constraints. For example, both bats and rats have evolved adaptations for nocturnal lifestyles, such as heightened senses of hearing and smell, which could have arisen independently in each lineage. Therefore, even if they evolved separately, bats and rats may still share similarities that place them within the nested hierarchy of life.
I don’t think we know enough about stem metazoans to make that judgement because they are still a subject of ongoing research and debate in the field of evolutionary biology.
For instance, the fossil record for stem metazoans is limited and controversial, with many early specimens difficult to classify and interpret. As a result, there is still much uncertainty about the timing and nature of their emergence, and ongoing research is focused on using genetic, biochemical, and morphological data to better understand the evolutionary relationships and characteristics of these early animals.
On the other hand, I doubt that primitive stem metazoans lacked those genes because molecular analyses have indicated that each major multicellular clade contains a characteristic set of developmental “toolkit” genes, some of which are shared among disparate lineages.
These toolkit genes are responsible for the development of various body structures and functions and are crucial for the evolution of multicellularity.
As further pointed out by Stuart Newman…
“Considering the shared and specific interaction toolkits of the various clades in relation to the physical forces and effects they mobilize helps explain how phyletically different organisms use genetically homologous components to construct phenotypically dissimilar but functionally similar (analogous) structures often without common ancestors exhibiting the character”.
The origins of multicellular organisms (uevora.pt)
Primary source:
Tetraspanin genes in plants - ScienceDirect
Algal Genes in the Closest Relatives of Animals | Molecular Biology and Evolution | Oxford Academic (oup.com)
I’m very familar, and I’m sure that Taq is too, with all of those. None of them demonstrate function.
How about answering my question above? I would think you’d have a strong opinion on it. I’ve quoted it below:
According to the selection-effect definition, you are correct, but as Manolis Kellis and his partners have pointed out:
"…there is no universal definition of what constitutes function, nor is there agreement on what sets the boundaries of an element. Both scientists and nonscientists have an intuitive definition of function, but each scientific discipline relies primarily on different lines of evidence indicative of function. Geneticists, evolutionary biologists, and molecular biologists apply distinct approaches, evaluating different and complementary lines of evidence.
The genetic approach evaluates the phenotypic consequences of perturbations, the evolutionary approach quantifies selective constraint, and the biochemical approach measures evidence of molecular activity. All three approaches can be highly informative of the biological relevance of a genomic segment and groups of elements identified by each approach are often quantitatively enriched for each other. However, the methods vary considerably with respect to the specific elements they predict, and the extent of the human genome annotated by each" [Emphasis added]
Defining functional DNA elements in the human genome | PNAS
No, it would not necessarily predict that there would be zero baseline, nonspecific binding if we test for transcription factor binding in vitro. In vitro experiments are conducted in artificial laboratory conditions that can often differ significantly from the in vivo environment. Therefore, it is possible that in vitro experiments may produce some degree of nonspecific binding or background noise.
However, a successful in vitro experiment would still demonstrate specific binding between the transcription factor and its DNA binding site, despite any background noise. The key point is that the presence of specific binding would support the hypothesis that the observed transcription factor-DNA interactions play a role in regulating gene expression in vivo.
Yes, “can.” As in not always.
You also didn’t list the first two in your list before. They’re much more informative. Have you considered reading and understanding before you quote?
As in no competition. I’m referring to studying binding that has already been observed in vivo.
No, you’re missing the point. It is certain that they do; thus binding itself is not an indicator of function.
No, you just missed the point I was making. Instead, my actual point is I am not arguing for one definition of function over another. There is no basis to exclude any of these definitions of function when it comes to evaluating whether the common design theory is validated or not. All contribute to our understanding of biological organisms as they pointed out:
"The biochemical approach for identifying candidate functional genomic elements complements the other approaches, as it is specific for cell type, condition, and molecular process. Decades of detailed studies of gene regulation and RNA metabolism have defined major classes of functional noncoding elements, including promoters, enhancers, silencers, insulators, and noncoding RNA genes such as microRNAs, piRNAs, structural RNAs, and regulatory RNAs (50–53).
"… Most data acquisition in the project thus far has taken the biochemical approach, using evidence of cellular or enzymatic processes acting on a DNA segment to help predict different classes of functional elements.
The recently completed phase of ENCODE applied a wide range of biochemical assays at a genome-wide scale to study multiple human cell types (69). These assays identified genomic sequences (i ) from which short and long RNAs, both nuclear and cytoplasmic, are transcribed; (ii ) occupied by sequence-specific transcription factors, cofactors, or chromatin regulatory proteins; (iii ) organized in accessible chromatin; (iv ) marked by DNA methylation or specific histone modifications; and (v ) physically brought together by long-range chromosomal interactions."
Defining functional DNA elements in the human genome | PNAS
Not necessarily. Although In vitro experiments can indeed show some degree of non-specific binding, this does not necessarily indicate that binding is not an indicator of function.
Firstly, it’s important to note that in vitro experiments may not fully represent the complex biological conditions in vivo, and the nonspecific binding may be less prominent or negligible in vivo.
Secondly, while nonspecific binding may be a technical limitation of the experimental approach, researchers can control for this by using appropriate experimental controls and techniques, such as mutant DNA sequences or competition assays, to ensure that the observed binding is indeed specific.
Finally, it’s important to consider the context in which the binding occurs. For example, if a transcription factor is known to be involved in a specific biological process and its binding is observed at a relevant DNA sequence in vitro, this may still indicate its functional role in vivo, even if some degree of nonspecific binding is also observed.
Therefore, while nonspecific binding may complicate the interpretation of in vitro experiments, it does not necessarily invalidate the role of transcription factor binding as an indicator of function in vivo.
And RNA polymerase also can initiate transcription spuriously on any site. To simplify, the transcription complex includes RNA polymerase and the initiation factors. The RNA polymerase by itself doesn’t bind very often to DNA, but sometimes it does and once bound it doesn’t very easily let go (this long-lasting binding is required for it to transcribe RNA). The holoenzyme (RNA polymerase + initiation factors) actually has very weak binding on random stretches of DNA, but strong binding when it finds a promoter. After that, the initiation factors disassociates and the RNA polymerase can do the job that requires non-specific binding on DNA. So the initiation factors reduce binding onto random DNA in favor of binding onto promoters. But note that occasional binding onto random DNA is not eliminated completely. And when we are talking about a cell that contains many thousands of these transcription enzymes “searching” for the occasional 100-1000 nucleotide long promoter among the 3.2 billion nucleotides, these enzymes are bound to spuriously transcribe a random stretch of DNA at least on occasionally. And when we are talking about human body with trillions of cells, it’s not surprising that most of the human genome will be occasionally transcribed simply due to spurious transcription alone.
Eh? Yes it does! The fact that spurious binding are able occur means that the mere presence of binding does not (in and of itself) indicate function. You have to separate the signal from the noise, but instead you will take any ‘sound’ as an indicator of signal, which is highly flawed or naive at the very least.
Oh, for Pete sake… literally… in the very NEXT paragraph in that paper:
An advantage of such functional genomics evidence is that it reveals the biochemical processes involved at each site in a given cell type and activity state. However, biochemical signatures are often a consequence of function, rather than causal. They are also not always deterministic evidence of function, but can occur stochastically. For example, GATA1, whose binding at some erythroid-specific enhancers is critical for function, occupies many other genomic sites that lack detectable enhancer activity or other evidence of biological function (70). Likewise, although enhancers are strongly associated with characteristic histone modifications, the functional significance of such modifications remains unclear, and the mere presence of an enhancer-like signature does not necessarily indicate that a sequence serves a specific function (71, 72). In short, although biochemical signatures are valuable for identifying candidate regulatory elements in the biological context of the cell type examined, they cannot be interpreted as definitive proof of function on their own.
Exactly what people here have been trying to explain to you, and yet… it’s in the very paper that you are citing. How about actually reading the whole paper instead of selectively quoting parts that you happen to agree with?
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No, you didn’t have a point.
But you are arguing that transcription-factor binding is sufficient. The ENCODE group was embarrassed into walking that back years ago.
There’s no theory. You don’t even have a coherent hypothesis.
Some contribute much more, as I’m pointing out.
None of that stopped at binding. Please stop pretending that you understand this.
Which was not very predictive. Have you considered putting data above words?
Yes, necessarily.
That is indeed an indicator.
ENCODE did none of that.
And you’ve reviewed how much of the primary literature in the field?
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As usual, you make no sense. If they evolved separately, we would not expect to see the nested hierarchy of genes found in vertebrates (e.g. 4 Hox clusters), sarcopterygians, tetrapods, amniotes, mammals, and eutherians, respectively. And we would not expect the sequences of those genes to reproduce the nested hierarchy. Nor would we expect, which was actually my point, for the common ancestor to have four Hox clusters, and in fact not even one Hox cluster, since you think the ancestor was a slime mold. Since those four Hox clusters evolved from one through two whole-genome duplications, there is no reason to suppose that some kind of loss was involved either.
Since this wasn’t an instance of gene loss, all you say is irrelevant. Note that gene gain also happens. The common ancestor of all metazoans did not have four Hox clusters.
We would not expect any such thing, and whenever you say “therefore”, it’s just a marker for a non sequitur. Four Hox clusters is a synapomorphy of vertebrates, and you can’t turn it into a primitive condition; too much independent and exact loss in other taxa would be needed.
Again, not true. Only if the primitive stem-metazoans had hair, mammary glands, and a four-chambered hears would we expect separately evolved descendants to possess those. It’s the ancestor of mammals, specifically, that had those characteristics. Again, it’s a nested hierarchy resulting from common descent.
There is no reason to expect similar adaptations to follow a consistent nested hierarchy, and many of the characters shared by mammals are not adaptive to particular environments. There’s no adaptive reason mammals should share 7 cervical vertebrae, for example, and it would even seem to be maladaptive in giraffes. There’s no reason mammals should share a phalangeal formula of 2-3-3-3-3, and certainly no reason the distribution of vertebral number and phalangeal formula should be the same. Only common descent explains that sort of thing, just as only common descent explains the Hox clusters. This is not a subject of which you have any understanding. This is not a subject you are willing to understand.
This is a common creationist trope, “If we don’t know everything, therefore we know nothing.” But it isn’t true. We know enough to know that stem-metazoans had only one Hox cluster, and most metazoans today get by with only that one.
All nice, but Hox clusters don’t fossilize. What we know about them comes entirely from comparative genomics. Your various quotes never mean what you think they do and never communicate a point you want to make.
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They identified DNA sequences that bind transcription factors. That’s not function. That’s binding.
None of which measures function.
They also bind to nonspecific DNA sequences that don’t regulate gene expression. That’s not function.
What percentage of the cell’s energy is used for non-specific transcription?
What would it take for absolutely zero non-specific binding, and how would that affect specific binding?
Baloney. Cells do it right now, and they don’t grind to a halt.
That’s word salad. It doesn’t mean anything.
HRT is not guided, nor is HGT.
You are claiming that HRT is guided BY A DESIGNER!!! You have not presented any evidence to back this claim.
You are claiming that a designer specifically interacts with nature, not fine tuning.
No, it’s not. Fine tuning is not guidance.
No, you didn’t.
Yes, you do.
None of which is required for function.
The hierarchal structure of transcription factors does not require a nested hierarchy of sequence between species. If you understood either concept you would know that. You are even citing HGT of transcription factors that violate a nested hierarchy.
Why does this require a nested hierarchy???
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Exactly. Here’s a quote I found over at Sandwalk that is quite instructive:
Non-specific binding and off-target activity is absolutely no surprise to people who work in these fields.
Not only no surprise, but ever present in the minds of anyone who has ever studied protein binding to anything.
Not only not surprising, and not only present in people’s minds, but absolutely unavoidable! You couldn’t not have spurious transcription given the way the system works.
Not only transcription, but translation. Most null mouse mutants don’t have a phenotype until long after (in the case of Myo5a, a month) both transcripts and protein are present in wild-type controls.
That’s not consistent with any design hypothesis. It is, however, a prediction of evolutionary theory–that turning things on is >100x more important than turning them off.
Would you mind sharing that math, please? How is importance measured, exactly, that makes such quantitative predictions about it possible to begin with, and how is the >100x factor arrived assuming principles of evolutionary theory?
I’ll do much better than that–I’ll point you to the evidence itself, so that you can count them up.
First, let’s make sure we are on the same page with Meerkat’s ID hypothesis (falsely presented as fact):
One can replace transcription with translation or energy consumption in that hypothesis. All three make clear empirical predictions.
Yes, I am arguing that but it is an inductive argument not a deductive argument, which means that there is a certain level of uncertainty in the conclusion.
The theory is just the modified version of Richard Owen’s common archetype theory.
Based on experiments and observations, I have already explained how we can infer that a personal agent not only chooses the right fine-tuning values for life to exist, but chooses the right genetic code for life.
This is why I defined the Universal common designer theory to be…The universal self-collapsing genetic code shown by the shared DNA among all living organisms (i.e., objective reduction).
The empirical prediction from this theory is finding non-random mutations in the non-coding regions of the genome, which has been labeled “junk DNA”, and in regions that do encode proteins but are primarily deleterious.
Well, I just laid out the universal common designer theory again . It is up to you now to explain how the other definitions of function contribute much more to our understanding of this theory.
Yes, thank you for making my point again. As I said before, a vast body of data demonstrates that transcription factors bind to specific DNA sequences that regulate gene expression. Even though another explanation for why these transcription factors bind to DNA may exist, future experiments can reduce this uncertainty.
The key point is this: There is nothing wrong with the reasoning the ENCODE Project employed to assign function to sequences in the human genome because they were making use of induction (as do all scientists), not deduction.
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.
Moreover, It is important to note that reducing non-specific binding does not necessarily affect specific binding. In fact, reducing non-specific binding can often increase the signal-to-noise ratio of an experiment, making it easier to detect specific binding. By minimizing non-specific binding, specific binding can be more easily distinguished from background noise.
You did not fully read the previous point I made in my long discussion with @T_aquaticus. For instance, a vast body of data demonstrates that transcription factors bind to specific DNA sequences that regulate gene expression. Even though another explanation for why these transcription factors bind to DNA may exist as you pointed out, future experiments can reduce this uncertainty.
The key point is this: There is nothing wrong with the reasoning the ENCODE Project employed to assign function to sequences in the human genome because they were making use of induction (as do all scientists), not deduction.
The very end of the paragraph in that paper reinforces this:
*In short, although biochemical signatures are valuable for identifying candidate regulatory elements in the biological context of the cell type examined, th ey cannot be interpreted as definitive proof of function on their own.
Exactly what I have been trying to explain to everyone, and yet… it’s in the very quote that you are citing.
How about actually reading the whole conversation instead of selectively responding and quoting parts that you think refute what I am saying ?
No, I actually don’t think it is a slime mold or a primitive stem metazoan. I just mistakenly called it a slime mold because I thought they represented what was considered to be the precursor or primitive form of multicellular animals. You also called them primitive stem metazoan, which made me think you were referring to fungi, brown algae, red algae, green algae, or land plants.
Now, if you are telling me that they are not considered to be primitive stem metazoans, then my mistake.
I was going off of molecular analyses indicating that each major multicellular clade contains a characteristic set of developmental “toolkit” genes, some of which are shared among disparate lineages.
These toolkit genes are responsible for the development of various body structures and functions and are crucial for the evolution of multicellularity.
These shared designs could have come from a last common ancestor, but they also could have came from HGT.
Algal genes in the closest relatives of animals - PubMed (nih.gov)
Either way, it does not necessarily conflict with the common design model.
According to the selection-effect definition, you are correct, but as Manolis Kellis and his partners have pointed out:
"…there is no universal definition of what constitutes function, nor is there agreement on what sets the boundaries of an element. Both scientists and nonscientists have an intuitive definition of function, but each scientific discipline relies primarily on different lines of evidence indicative of function. Geneticists, evolutionary biologists, and molecular biologists apply distinct approaches, evaluating different and complementary lines of evidence.
The genetic approach evaluates the phenotypic consequences of perturbations, the evolutionary approach quantifies selective constraint, and the biochemical approach measures evidence of molecular activity. All three approaches can be highly informative of the biological relevance of a genomic segment and groups of elements identified by each approach are often quantitatively enriched for each other. However, the methods vary considerably with respect to the specific elements they predict, and the extent of the human genome annotated by each" [Emphasis added]
Defining functional DNA elements in the human genome | PNAS
Simply because evidence is consistent with an alternative hypothesis does not mean that it falsifies the original theory. In science, it is not enough to merely show that a theory is consistent with one set of observations; the theory must also make testable predictions that can be verified through experiments or observations.
For a theory to be considered falsified, it must make a prediction that is not consistent with the evidence. If the evidence is consistent with both the original theory and an alternative hypothesis, then the original theory may still be valid, but further testing may be needed to distinguish between the two hypotheses.
In summary, falsifying a theory requires evidence that is inconsistent with the predictions of the theory, rather than just evidence that is consistent with an alternative hypothesis.
It is estimated that in Escherichia coli, non-specific transcription accounts for approximately 20-30% of the total energy consumption during steady-state growth. This is due to the fact that non-specific transcription can lead to the production of unnecessary proteins, which can then require additional energy for degradation.
However, it is important to note that this estimate is specific to E. coli and may not be applicable to other organisms or cellular contexts. Furthermore, the exact percentage of energy used for non-specific transcription can be difficult to measure and can depend on many factors, including the specific genes being transcribed, the rate of transcription, and the energy efficiency of the transcription machinery.
Achieving absolutely zero non-specific binding is likely impossible, as all binding events involve some level of non-specific interaction. However, reducing non-specific binding to an extremely low level can be achieved by optimizing experimental conditions and using appropriate controls.
Non-specific binding can occur due to electrostatic interactions, hydrophobic interactions, or non-specific interactions between biomolecules. To minimize non-specific binding, researchers can use blocking agents, such as bovine serum albumin (BSA), or specific inhibitors to target non-specific interactions. Additionally, optimizing the pH, ionic strength, and temperature of the reaction environment can also reduce non-specific binding.
If non-specific binding were completely eliminated, it would likely result in a significant increase in specific binding. This is because non-specific binding can interfere with the binding of specific molecules, leading to decreased sensitivity and specificity in experimental assays. By reducing non-specific binding, the signal-to-noise ratio of an assay would increase, resulting in improved detection and quantification of specific interactions.
However, it is important to note that complete elimination of non-specific binding may not be desirable in all experimental contexts. Non-specific binding can sometimes provide useful information about the specificity and selectivity of a biomolecule, and complete elimination of non-specific binding could lead to an oversimplification of complex biological interactions. Therefore, the level of non-specific binding should be optimized based on the specific goals and requirements of the experiment.
Yes I did :
Incongruence between phylogenies derived from morphological versus molecular analyses, and between trees based on different subsets of molecular sequences has become pervasive as datasets have expanded rapidly in both characters and species. 1. Liliana Dávalos et. al, “Understanding Phylogenetic Incongruence: Lessons from Phyllostomid Bats,” Biological Reviews of the Cambridge Philosophical Society 87 (2012), 991–1024, doi:10.1111/j.1469-185X.2012.00240.x.
Are you kidding me? So If I say that we are all living in the matrix, this means that you and everybody else would have the burden of proof to refute this claim?
As I mentioned before, the genetic code is the same for all living organisms, and variations in the code are responsible for differences in traits between organisms. As organisms evolve and diversify, the genetic code is inherited and modified through a process of HRT, resulting in the formation of new species and groups of organisms.
This process of HRT creates a nested hierarchy of organisms based on their shared design and the extent of their genetic similarities. Organisms that share more recent common design will have more similarities in their genetic code and will be grouped together in smaller, more closely related categories, while organisms that diverged from a common design further back in time will have more differences in their genetic code and will be grouped together in larger, more distantly related categories.
Why were these numbers chosen rather than some other numbers?
Patel showed how quantum search algorithms explain why these numbers were chosen. [22] To summarize, if the search processes involved in assembling DNA and proteins are to be as efficient as possible, the number of bases should be four, and the number of amino acids should be 20.
An experiment has revealed that this quantum search algorithm is itself a fundamental property of nature.
In other words, to address a common set of problems faced by organisms possessing different characteristics and living in different habitats, this single optimal solution must be employed.
This is why a nested pattern is a necessary consequence of the process of evolution and common design. It provides a clear and systematic way of classifying and understanding the diversity of life on Earth.
Again, the observations and experiments I just described above justify defining it that way.
The definition of consciousness is self-collapsing wave-function. Since there is a quantum basis for the genetic code, we can extend this definition to biology and call it Self-collapsing genetic code.
How does this support the point you made before?
You said there is no reason why this would produce a nested pattern. Now, it looks like you acknowledge that it does.
The article “Natural engineering principles of electron tunnelling in biological oxidation–reduction” published in Nature discusses the role of electron transfer in biological oxidation-reduction reactions, specifically focusing on the principles of electron tunnelling.
The principles of electron tunnelling discussed in the Nature article are relevant to HGT because they provide a framework for understanding the evolution and adaptation of electron transfer systems in organisms. Electron transfer systems are essential for many biological processes, including respiration, photosynthesis, and nitrogen fixation, and they are often subject to horizontal transfer events that can introduce new variants or modify existing systems.
The article discusses how the natural principles of electron tunnelling can help explain the efficiency and selectivity of electron transfer reactions in biological systems, and how these principles can guide the design and engineering of synthetic electron transfer systems. By understanding the fundamental principles of electron transfer, researchers can gain insights into the evolution and adaptation of electron transfer systems, including those that are horizontally transferred between organisms.
Natural engineering principles of electron tunnelling in biological oxidation–reduction | Nature
Based on the quantum mind theory, I have already explained how it does. Here it is again…
According to Roger Penrose, the action of consciousness proceeds in a way that cannot be described by algorithmic processes. [8] For instance, conscious contemplation can ascertain the truth of a statement and freely make intellectual and moral judgments. This involves distinguishing between true and false statements or what is morally “right” versus “wrong.”
The only thing in nature that does this is a wave-function collapse. For instance, at small scales, quantum particles simultaneously exist in the superposition of multiple states or locations, described by a quantum wave function. However, these superpositions are not seen in our everyday world because efforts to measure or observe them seemingly result in their collapse to definite states. [5] Why quantum superpositions are not seen is a mystery known as the measurement problem, which seems somewhat related to consciousness. Experiments from the early 20th century indicated that conscious observation caused superposition wave functions to collapse to definite states, choosing a particular reality.
Here is an example: “
No naive realistic picture is compatible with our results because whether a quantum could be seen as showing particle-like or wave-like behavior would depend on a causally disconnected choice” [21]
https://www.pnas.org/doi/10.1073/pnas.1213201110
Consciousness was said to collapse the wave function under this view. [5]
Moreover, Diederik Aierts [9] demonstrated how these two phenomena are identical by applying the quantum theory to model cognitive processes, such as information processing by the human brain, language, decision-making, human memory, concepts and conceptual reasoning, human judgment, and perception. Owing to its increasing empirical success, quantum cognition theory has been shown to imply that we have quantum minds.
Other empirical data have shown that the brain is a quantum computer that uses quantum mechanical processes, such as quantum tunneling and superposition, [10, 11] explicitly suggesting that we have quantum minds, as the Orch-OR theory predicted (Read section 4.5 OR and Orch-OR of “Consciousness in the universe” by Hammeroff and Penrose for more details). [12]
Overall, this means that we can infer that a personal agent not only chose the right fine-tuning values for life to exist, but chooses the right genetic code for life.