Looking for sources on the information argument continued

Continuing the discussion from Looking for sources on the information argument:

Stop saying nonsense please. Look at the two sequences, from two parents, below:

Both recombine during meiosis to yield:

Hasn’t the natural process of homologous recombination specified the exact order of nucleotides in the DNA of their child?

Now you have switched to abiogenesis. In any case, natural processes can satisfactorily explicate the precise order of nucleotide bases in extant organisms which was what you initially disagreed with. If you meant something else and we responded with something unrelated, blame your poor expression of your intent for that.

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What is satisfactory to you many not be satisfactory to others.

While you can explain sequence 1 and 2 combined you have not explained the origin of 1 and 2 separately. This is not only an origin of life discussion as we see many new unique genes in different animal types.

Parental sequences 1 & 2 derived from the DNAs of the child’s grandparents (their own parents). Seems like you have forgotten how transmission genetics works.

New, unique genes can arise de novo, via divergence following duplication, via fusion, via point mutations, via insertions and deletions of DNA segments, via horizontal gene transfer etcetera.

Before you go on harping about a model to account for this, remember Rumraket shared a paper showing a pretty comprehensive model on de novo gene evolution. There are also papers for models involving gene duplications and fusions. Have you read these papers?

By “satisfactory” I mean we know mechanisms that can completely account for a lot of biological phenomena or structures, rendering unsupported claims of intelligent design unnecessary.

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Thats right but still does not explain the original origin of the information. You cannot assume it is the origin of life. It may have originated after.

Rum understands the weakness of the model as it is based on the Fisher Wright model which occurred before we knew the make up of the transcription translation mechanism. Function comes before fitness. Function in living organisms is initiated by a sequence.

Intelligent design is necessary as a counter hypothesis. You are making claims that are not tested according to the scientific method. What else will keep your wonderful imagination in check :slight_smile:

DNA and proteins are functional sequences. Functional sequence space by definition is smaller than total sequence space. When you change it randomly information entropy will move it toward non function over time. You can find thousands of papers in pubmed that will show how this works such as cancer caused by mutation.

Contrary to the paper cited we now know most mutations are deleterious. This is logical mathematically based on what we know about functional sequences.

https://doi.org/10.1111/j.0014-3820.2003.tb01561.x.

Oh, the irony.

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The origin of genomes be it DNA or RNA go back to before LUCA. This is not an assumption. Its in the data you don’t bother checking.

You really love to embarrass yourself by putting up your ignorance for all to see. Tell me what translation and transcription have to do with the Wright-Fisher model? Do you even know what the Wright-Fisher model is?

And fitness preserves function.

Look at the evolutionary biology literature, do you see ID being used for anything? Look at the ID literature, do you see anything that provides evidence for ID claims? The answers to both questions is a big NO! ID is useless.

Read papers on molecular evolution and you will see gene duplication, fusion, exaptation, mutations etcetera mentioned or investigated as mechanisms for the origin and evolution of biochemical structures and systems. You don’t see ID, because it is a vacuous and practically useless idea. More importantly, ID ideas like the inability to evolve irreducible complexity have been beaten to death. I repeat, ID is bunk and offers no help to biological research.

Be rest assured my thoughts are in line with current evidence. You, on the other hand, has refused to exit your fantasy world.

Not all DNA sequences are functional. For example, during mRNA processing, introns are removed and degraded by nucleases simply because they serve no function in the protein or RNA molecule to be derived from the stitched up exons. Similarly, not all protein sequences are functional.

Don’t you see this is contradictory? If randomly changing DNA inevitably moves it towards nonfunctionality, then cancers should not exist since they make their metabolic machinery hyperfunctional to sustain their abnormal way of life.

For example, mutations to the receptor for the Epidermal Growth Factor (EGF) protein can permanently activate the receptor even in the absence of its stimulatory signal (EGF protein). This hyperfunctional receptor protein goes on to drive tumorigenesis.

So you are now an advocate of neutral theory. Great. However, you misunderstand it.

Neutral theory states that most mutations which affect fitness are deleterious, making purifying selection the predominant mode of natural selection as it moves to eliminate these deleterious mutations. In addition, a large fraction of genomes like ours are evolving by genetic drift because mutations that affect those parts are effectively neutral. If these parts are neutral, then they are most likely nonfunctional (junk DNA). For example, most introns accumulate substitutions a lot faster than the exons they separate since they are nonfunctional.

Do you accept a large portion of your genome is junk, since it is beset by a lot of neutral mutations? (Remember you are now an advocate of neutral theory). :laughing:

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Sure but not the modern genes we are observing.

The Wright Fisher model came before transcription translation was understood which signify that genes are sequence based. The model does not take into account deleterious mutations that are prevalent in functional sequences.

I have seen modifications from ID’s influence.

This is a statement due to your anti ID bias. It’s a useful scientific method for investigating the limits of science.

The mutations put the cell out of regulation ultimately killing the organism if not treated. Loss of regulation is loss of function.

What I think is we need to look at both sides of the arguments. I think the amount of function in our genome is yet to be discovered.

The measurements are difficult because transcription varies depending what stage of the organisms life cycle you are measuring.

Do you accept most the genome is Junk DNA? What evidence do you base this hypothesis on?

I haven’t. Please cite them.

Remember, ID could have had its moment in the sun to address the question, “Was SARS-CoV-2 designed?” That would seem to be a softball given how IDcreationists have been telling us how great they are at “detecting design,” but they were nowhere to be seen, except for relaying the right-wing disinformation about the pandemic.

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Some extant genes are orthologous, while others arose within specific lineages following common descent through a number of mechanisms we have told you a lot of times.

Pure rubbish. Try again. How does translation and transcription undercut the Wright-Fisher model of population genetics?

If you don’t understand the paper just tell us, instead of saying extremely silly things.

I knew it. You don’t understand the Wright-Fisher model. Keep embarrassing yourself.

Citations?

There is no bias here. Its facts. Please find me one research article in evolutionary biology where ID was used to investigate anything and falsify my claim. As far as biological research is concerned ID is useless.

Facepalm!

You just claimed that altering the information content of DNA will inevitably lead to nonfunctionality. Cancer cells refute this foolish claim of yours because their genomes suffer a bewildering number of genetic changes (of all kinds), yet the metabolic machinery that sustains them goes into overdrive because of these mutations. Do you now agree that you made a bogus claim?

Loss of regulation does not necessarily involve loss of function. In the example I gave, the function of EGF receptor is to stimulate cellular division via a signalling cascade. In some cancers, this receptor acquires substitutions that make it permanently actively. That is not a loss-of-function, but a boost-of-function. You fail at population genetics, now you fail at biochemistry.

Don’t change the subject. You cheerily linked to a paper coauthored by Lynch, wherein he mentions that most mutations affecting fitness are deleterious, a core tenet of neutral theory. Under Neutral theory, portions of genomes that do not affect fitness are nonfunctional, and so evolve by genetic drift. A large fraction of the human genome is under evolution by drift, that is, those regions are junk. If you don’t accept this, then why did you cite the Lynch article discussing Neutral theory?

Please if you don’t have any meaningful thing to say, just stay quiet.

A large fraction of our genome is junk. If it wasn’t, events like nonhomologous end-joining, DNA replication errors etcetera would leave most of us dead.

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A good story but not a tested hypothesis.

This is not an argument. Are you claiming that the model takes deleterious mutations into account based on current empirical evidence? The Fisher Wright model is not based on current empirical evidence.

I think you confuse a fact with an untested hypothesis.

When a cell is dividing when it should be in stasis it is out of regulation. Multicellular organisms cells need to have different rates of division dependent on the maturity of the organisms.

So you are going to pretend I haven’t shown you experimental verification of one or more of this mechanisms generating new genes in lineages that descend from an ancestral population in another thread?

You don’t understand the Wright-Fisher model. You don’t understand anything.

You claimed translation and transcription undercut the Wright-Fisher model, how?

In addition, there is a version of the Wright-Fisher model that takes selection (hence, beneficial and deleterious mutations) into account alongside other evolutionary forces like genetic drift.

More importantly, that paper describing a model for de novo gene evolution takes into account, the effects on fitness by the mutations that appear in every generation. Did you not read this section of the paper:

Like I said, if you did not understand the paper, tell us and stop embarrassing yourself.

In its simplest form, the Wright-Fisher model is an idealized one. It assumes no selection, no migration and purely random mating, conditions that do not hold in real life. In a sense, it is like the ideal gas law in chemistry in its simplest form. The model is pretty useful until its assumptions are strongly violated. That’s why there are versions of it that take selection, migration etcetera into account. Just continue showing us how clueless you are.

Its a fact that ID is completely useless to evolutionary biology research. To falsify my claim, provide me one paper that shows otherwise. Spoiler alert: there is none!

I take it you now see the vacuity of your claim that mutations in DNA inevitably lead to nonfunctionality, considering your response doesn’t address what I said and was borne out of the need to say something even if it irrelevant. Cancer cells with hyperfunctional systems due to multiple mutations demolish your claim that mutations in DNA ratchets it toward nonfunctionality.

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What do you think experimental verification is? Testing if the model with its assumptions works? What happens when the assumptions turn out to be unrealistic?

These are things you need to say when you don’t have an argument. Your opinion of what you think I understand is of no consequence.

What it does not take into account is the journey (trials through a sequence to find function) from non function to function which must be established to have feasible waiting times.

From the paper:

Our approach is therefore immensely simple, but it comes with trade-offs;importantly, this framework cannot capture non-adaptive aspects of genome evolution. For example, we cannot test here the role of pre-adaptation, which is a non-adaptive process that leads to sequences evolving away from highly deleterious phenotypes, but does not prescribe whether and how sequences gain new functions (Masel, 2006). Nevertheless, an advantage of the present framework is the multitude of experimental studies that measure organismal fitness in terms of an easily accessible, universal quantity: the relative growth rate

This is right. A model must be tested against real world conditions. If this model is to work non coding DNA sequences must be pretty close to function or the waiting time will be very long. So far this has not been experimentally verified.

In this case, a demonstration of gene duplication, recombination, fusion and other mechanisms producing new genes as lineages diverge following their split from a common ancestor.

No. I am talking about the mechanisms I mentioned above generating novel genes.

Very simple models usually start with unrealistic assumptions and are used until they begin to perform suboptimally. At that time more complexity is built into the model by having it work with more realistic assumptions. In a lot of cases, these refined models with more realistic assumptions work a lot better. The Wright-Fisher model has an extremely simple form and also very complex ones. These complex Wright-Fisher models incorporate selection, migration, and other real life factors ignored by the simple version.

If you don’t understand what you are trying to critique, you will always criticize a strawman version of that thing which is what you are doing. You have failed at understanding simple biochemistry and population genetics.

Thanks for clearly demonstrating you don’t know what you are talking about. Wright-Fisher model is a POPULATION GENETIC MODEL TRYING TO UNDERSTAND HOW ALLELES TRANSMIT ACROSS GENERATIONS IN A POPULATION UNDER CERTAIN CONDITIONS. It is not a model for searching or navigating through sequence space.

In general, fitter mutants will have a higher probability of passing on their genes to progeny and vice versa for less fit mutants. According to the paper, if the average fitness supersedes some genic threshold, then a new gene has been born as the new gene beneficial function raises the average fitness of individuals who have it over their current genic threshold for fitness. This is why it used the Wright-Fisher model because it can help model the allelic transfer dynamics.

Like I said, you keep saying what you don’t understand.

You are beginning to annoy me. The part you quoted and bolded has nothing to do with searching through sequence space and its about preadaptation, a nonadaptive process. The model’s weakness is its ignorance of nonadaptive mechanisms of genome evolution. It considers just adaptive forces generating new genes. Again, you are demonstrating your cluelessness here.

Haven’t you been listening to me? There are Wright-Fisher models with more realistic assumptions and they are pretty good at what they do in many cases.

It took two weeks for E.coli to evolve new promoters to facilitate expression of some of its genes under selection. This waiting time problem only exists in your head.

Rubbish.

https://www.nature.com/articles/s41467-018-04026-w

I am done with you. For now.

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Your experiment covers most of biodiversity? E coli and a promoter region solves the waiting time problem searching through a sequence to find function across a diverse set of organisms? You are not following the conversation as I made being close to function a necessary requirement. All you have shown here is promotion can be close to function. There needs to be a reason most NC DNA is close to function.

The challenge that stimulated the study is the quantity of orphan genes that are being discovered. For the LUCA of LVCA hypothesis to be considered a real model needs to be developed or the hypothesis needs to be changed.

For this the idea that improved fitness through DNA mutation moves you toward complex function would need to be established. From the basic structure of DNA and the transcription translation mechanism generating proteins this does not look feasible without unreasonable assumptions.

E.coli is a model organism and in many cases its evolutionary dynamics are similar to ours or to any other life form on the planet. Much of biology owes its advances to experiments with E.coli.

Didn’t you read the abstract? Look at it again:

Not surprisingly, there is massive experimental support for this. One of my recent favorite papers (thanks to Rum) discusses this in depth:

You are the one who has been talking nonsense all along. You are yet to explain how translation and transcription affect the Wright-Fisher model. You also have not admitted that you wrongly thought the de novo gene birth model paper did not consider deleterious mutations when it clearly did. You also have not admitted that you were wrong about mutations inevitably leading to nonfunctionality. I noticed you quietly stopped mentioning these things, but it’s pointless as you have sufficiently demonstrated your ignorance on those topics.

First, I don’t know where you got the idea that “most NC DNA is close to function”. That should be “some” not “most”, unless you have somehow quantified that.

Second, what the paper I cited showed was natural selection acting to preserve and improve new functions. In most cases, the newly formed promoters showed little expression, but thanks to the interplay of mutations and selection the promoter function steadily improved until its expression was comparable to the wild-type promoters. From the paper:

We have given you a paper with a real model that shows how new genes are born de novo, but unfortunately, you don’t understand it. We have given you papers showing how gene duplication can give rise to novel genes or genes with novel function, but you don’t understand them. You are wasting our time.

This has been established and shown to you so many times. That promoter paper is one of them. In about 60% of the random sequences, it took one mutation to establish a weak promoter function and with further mutations (increasing complexity) this function was gradually improved.

Back with your rubbish eh? Explain how transcription and translation affect the de novo gene birth model?

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This mechanism and its detailed discovery showed DNA is a code.
One of the functions of that code is to translate to proteins. Long stretches of code live in almost infinite mathematical space because of the laws to combinatorial mathematics and exponential mathematics.

The size of the sequence space is not disputed as it is mathematically calculable as the number of possible characters in the sequence (N) to the power of the length of the sequence. What is disputed is the number of solutions or functions contained in the sequence (L). Sequence space = N^L

This all was discovered after the fisher wright model was formed. Since then empirical evidence has shown by the Michael Lynch paper I cited earlier is that most mutations are deleterious. This is a logical consequence of a functional sequence living in almost infinite mathematical space.

The paper that @Chris_Falter cited does not take this issue into account and as I cited above the authors understand this is a limitation of their model. The discovery of the transcription translation mechanism and that DNA is a translated code is an observation that provides one of the strengths of the ID argument.

To translate this argument into Mike Behe’s language DNA and its subset genes are a purposeful arrangement of parts. The purpose is to build a unique set of animals like the ones we are observing in nature.

What mechanism? What detailed discovery?

Biochemistry fail: DNA is not a code. It is just a polynucleotide with a 2’-deoxyribose sugar.

Biochemistry fail: ribosomes catalyze protein synthesis not DNA.

Irrelevant to evolutionary biology. Extant genomes are the products of billions of years of evolutionary change through the mediation of evolutionary mechanisms, not purely random searches through sequence space.

What was discovered?

Neutral theory fail: you misunderstand Lynch gravely. According to Neutral theory which Lynch was talking about, most mutations that affect fitness are deleterious. Read:

The mostly deleterious nature of fitness-affecting mutations is a consequence of Neutral theory not the nonsense you wrote above.

Biochemistry fail: DNA is not translated code. It is not even translated at all. You are unbelievably dumb.

Explain how transcription and translation support ID arguments?

Biochemistry fail: DNA doesn’t build anything. It can’t even build itself and requires the action of a good number of proteins for that purpose.

I’d advise you stopped embarrassing yourself.

PS: I just added the source for my quote on neutral theory.

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This is from Lynches paper.

In summary, the vast majority of mutations are deleterious.

This is one of the most well-established principles of evo-

lutionary genetics, supported by both molecular and quan-

titative-genetic data. This provides an explanation for many

key genetic properties of natural and laboratory populations.

Here is a table of the genetic code for proteins. It is made of DNA nucleotides.

Let’s start from here. What is your disagreement with a RNA Condon such as GUU (nucleotides above) coding for the protein valine? I understand transfer RNA and the ribosome are involved in translation but the genetic information (genetic code) is stored in DNA prior to transcription into RNA.

Do you disagree with this?

Actually, it did. @Michael_Okoko quoted the passage describing how they took it into account.

The passage you quoted, Bill, has to do essentially with the effect of drift. Not at all the same thing as the fixation of deleterious mutations, which is the subject of Lynch’s papers.

Lynch cannot be understood unless you take into account–as Lynch did–the effect of purifying selection.

Present tables that incorporate purifying selection into account, and we’ll have something to discuss.

Best,
Chris

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That paper is literally titled:

TOWARDS A REALISTIC MODEL OF MUTATIONS AFFECTING FITNESS

For the sake of emphasis, look at the title in a screenshot:

Lynch is operating from Neutral theory and according to it, fitness-affecting mutations are mostly deleterious. This shouldn’t confuse you.

In the human genome, for example, there are ~20,000 protein-coding genes. That’s just 1% of the entire human genome. Then there are RNA-coding genes as well and when we add them up with protein-coding genes, they constitute <3% of the genome. Not of all these genes are essential, but let’s pretend they all are, and so they determine the fitness of the individual who carries them.

Here comes the key point. Lynch is saying that most mutations that affect these genes (which determine how fit an individual is) are deleterious. In addition to genes, there are other parts of the genomes that influence fitness like gene regulatory regions. Mutations that affect all of these place are mostly deleterious. That’s all Lynch is saying.

We can try to evaluate how much of the genome is affected by non-neutral/fitness-affecting mutations or neutral ones. In humans, a huge portion of our genome is neutrally evolving, as the vast majority of fixed substitutions (scattered over the entire genome) are selectively neutral. Thus, most mutations that affect us are neutral, but most that affect the fitness - determining regions (which are tiny) are deleterious and are purged by purifying selection.

Biochemistry fail: that table shows RNA nucleotides not those of DNA.

Its codon not “condon”.

I have never disagreed GUU codes for valine. That you even think I said or implied this further demonstrates you are completely out of your depth here.

Biochemistry fail: that table is the genetic code. I repeat, the table is the genetic code. The genetic code is not stored in DNA, rather the information in the form of codons that is stored in DNA can be “decoded” using the genetic code (the table). Continue embarassing yourself.

You should disagree with many of the things you wrote because they are a strawman version of basic molecular biology and biochemistry.

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