u/Ill_Impact6838

Creationists still bring up Levinthal's paradox to falsify evolution. They say a functional protein of 50 or 100 amino acids will take billions of years to evolve and fold to perfect 3d shapes , so if it takes so much time for a single protein to evolve to be useful ,then how evolution creates so many proteins ? How ?

Well they don't know about energy funnel concepts,which describes that protein folding is not completely random and it's guided by physics and chemistry. Hydrophobic regions will always prefer to hide from polar aqueous environments ,hence making it possible for mostly polar groups to stay exposed to polar environments.

And if they really deny protein evolution ,how come can they accept that bacterial antibiotic resistance genes like beta lactamase have undergone mutations in so many different bacterial species or strains over the years ? There's so many varied sequences of beta lactamases.

Like you all accept that bacterial antibiotic resistance is natural ,right ?

Who is Sal Cordova?

I have heard his name before , but don't know the type of arguments he uses. Can u all pls help me here ? Student of microbiology here,as I mentioned before about myself. So yeah , I will understand the things he says related to my field of study. I have heard that some say he is a liar and all , but why ?

What are the arguments he uses ?

So this is the last part of my response to James Tour's video - Evolution vs design

Here , Onsi Fakhouri shows a slide where he writes the following things and reads it -

1)Features of life that are far from optimal or claimed to be junk are used as evidence for evolution.

How can this same process also be responsible for such exquisite optimality? If evolution is capable of producing all possibilities, then how is it a useful theory?

2)Claims that evolution could be a grand optimizer are rarely accompanied by quantitative prediction.

As Bialek points out: this is hard and seemingly intractable.

3)There are reasons to doubt that evolution can produce such exquisite optimality.

Marginal selective effect seems low and lost in noise, and such over-fitting requires a fixity; a commitment to an approach which could be only a local fitness maximum, and inability to adapt from there.

My responses -

1)His points are kinda absurd. Evolution can explain origin of junk ,optimal and sub optimal traits .

Evolution is highly useful because it predicts exactly when each outcome will happen based on measurable genetic and environmental factors.

Optimality is predicted when a population experiences intense, unchanging selection pressure over millions of generations.

Suboptimality is predicted when an organism shifts to a new lifestyle but is structurally restricted by its inherited ancestral DNA. For eg- RubisCo enzyme which captures atmospheric co2 and convert it into sugars during photosynthesis. Rubisco is slow and also 25% of times it captures o2 instead of CO2 , hence creating a toxic byproduct called 2 - phosphoglycolate. Photosynthetic organisms have to spend extra energy to remove this toxic byproduct.

Why did this occur ? Bcoz this enzyme evolved 3 billion years back when there was no o2 in environment. Later these organisms flooded the atmosphere with o2 .By the time o2 flooded the atmosphere, Rubisco’s active site was already locked into a foundational biochemical architecture that could not be easily overhauled without risking cell death.

Suboptimal traits can occur also due to genetic constraints ,like antagonistic pleiotropy, a gene responsible for a highly beneficial trait at one stage of life can impact this same organism's survival negatively at its another stage of life .

Genetic inbreeding can also lead to formation of sub optimal traits , like cheetah ,which suffered population crash many years back. Now nearly all of the surviving ones are genetically identical,having weak immune system , fertility issues etc.

Junk traits like Gulo pseudogene can be explained due to environmental relaxation on selection . Since our early ancestors used to feed on vitamin c rich foods , there was and is no problem with this gene's inactivation. But if humans live in an environment where there's no access to such foods ,then diseases like scurvy and even death can occur .

The theory is strictly testable because it predicts that even the most "optimized" traits will still contain structural defects or remnants inherited from ancestral blueprints.

2. When physicists and biologists like William Bialek state that tracking or modeling evolution is "hard and seemingly intractable," they are referring to a mathematical and computational challenge, not a statement that the process does not happen.For example, a tiny protein made of just 100 amino acids has more possible structural combinations than there are atoms in the observable universe. Predicting exactly which mutation a species will get next out of billions of possibilities is mathematically "intractable." However, acknowledging that a system is chaotic and difficult to simulate does not mean the system isn't real.

By this logic ,even weather is difficult or impossible to track ,does it mean weather doesn't exist ?

3)Mathematical biology proves that natural selection successfully filters out random genetic noise over long time scales.

The Rule is that a mutation providing a reproductive advantage as tiny as 1% (s = 0.01) is mathematically guaranteed to spread and become fixed in a population, provided the population is large enough. The strict biochemical rule is that if the effective population size (N_e) multiplied by the selection advantage (s) is greater than 1 (N_es > 1), natural selection overrides random genetic noise and permanently preserves the trait.

A mutation with a 0.001% advantage happens thousands of times over millions of years. Eventually, by pure statistical chance, one instance survives initial random deaths.Individuals with the mutation reproduce slightly more successfully, passing the gene to more offspring each generation.Once hundreds of individuals carry the mutation, random events can no longer wipe it out.

Also, genomes and environments are dynamic, meaning species are never permanently stuck at a single structural limit.

Ecosystems change constantly. A physical trait that was a "local peak" under dry conditions becomes a disadvantage when humidity increases, completely altering the fitness landscape and forcing new genetic variations to emerge.

I am disappointed with with whole batch especially James Tour. When everyone mocked him at one time , I still gave him a pass ,but now I understand why it's so easy to get frustrated with him. The guy isn't doing science. He is following an agenda. His channel is full of misinformation.

Like how are you talking about evolution when you urself are not qualified? Then ,you are bringing people who also don't know about it. You are bringing chemists , software developers in your channel, talking against evolution. Wth?

Btw ,what do you all think about Onsi's statements?

So , this is the third part of our debunking of their video - Evolution vs design.

And this part clearly shows that no one should take these people seriously. I mean they don't understand how biology or evolution works.

So first , onsi referenced Stuart Burges who says human foot is an extremely optimum multifunctional system. And it's designed. Also he says that knee joint is exquisitely optimal in its design( even though in reality it's one of the most injury prone body part of our body ) , he also talks about eye design ,how complicated it is , and middle ear.

If anyone can respond to this paragraph then it will be good. Since anatomy is not really my subject hence those who know about this can debunk the things said by Onsi .

But the funniest things are these claims-

1)The trochleal pulley along with oblique muscles in the eye is perfectly designed, it's irreducibly complex, it just made me say ,hey god ,how amazing you are !- who said this ??? Dr. Rob Stadler.

My response is - No , the oblique muscle is extremely old . In fish and shark,they have the oblique muscles but they lack the trochleal pulley. Infact it evolved later in land animals . So no , it's not irreducibly complex. Also in embryological development,the muscles arise first ,then comes the pulley.

2. Next Truman says that a mutation needs to happen in sperm for this ,and then this system needs to spread simultaneously or independently in both the halves of the body ( eyes) ,which is impossible to do for evolution.

Nope , the instructions are written once , but read twice ,any alterations in the sperm having instructions for eye development will be read twice ,once in each half . In easy words ,he is assuming as if both halves need to undergo mutations independently .

3. Rob says that any changes to the embryo is deleterious. And also he points out embryo development mechanism differ in drosophila and c elegans,even though they share common ancestor. To which James say ,then the theory should be blown away.

In reality, the entire field of Evolutionary Developmental Biology (Evo-Devo) shows that embryos can easily survive specific types of genetic changes.

Rob assumes mutations must destroy a developmental pathway. However, many mutations simply tweak the timing (heterochrony) or the amount of a protein produced during growth.

If a mutation completely deletes a gene required to make a heart, the embryo dies.

But if a mutation simply causes a bone-growth protein to stay active for 5% longer, the embryo survives perfectly fine. The only difference is that the adult will develop a slightly longer limb or a differently shaped jaw.

Embryos are Modular (Built in Separate Compartments)

Embryonic development does not happen as one single, interconnected chemical reaction. It is modular, meaning different parts of the body are built by independent genetic networks.

The genetic instructions used to build a limb are separate from the instructions used to build the liver or the heart.

Because of this modularity, a mutation can alter the shape, size, or structure of a limb or an eye socket without affecting the vital internal organs. The embryo stays alive because its essential life-support systems are completely untouched by the mutation.

For eg- All dogs belong to the exact same species, yet a Chihuahua looks completely different from a Great Dane. These differences in skull shape, leg length, and body size are caused entirely by mutations that altered how their embryos grew in the womb. None of these embryonic changes killed them.

If creationists like him accept that dogs evolved ,then he should not have spew out this garbage.

And regarding C elegans and Drosophila , both shared a common ancestor some 600 mya back ,but they still share the basic regulatory genes ,i.e. Hox genes . Hox genes only provide positional data late in development. C. elegans and Drosophila look entirely different because the early maternal genes, the physical cell structure (isolated cells vs. a shared fluid environment), and the exact number of Hox genes differ completely between the two organisms.

And James Tour should stop acting like a dumbo.

Anyways ,part 4 is going to be the finale of this video and will be launched soon.

What do you all think about their claims . Also , pls someone tell me about Onsi's points on anatomy, in detail , regarding Knee joint, foot.and middle ear . I am eagerly waiting.

Hello everyone,we are covering James Tour's video titled - Evolution vs design

In last part , I covered on the topic signal network and how they were whining that such a complicated system of embryo formation in fruitfly couldn't have evolved naturally .

In second part , I am going to talk about their second point, TADs ( Topologically Associated Domains)

Here are the exact points regarding TADs (Topologically Associating Domains) they talk about

1. TADs refer to groupings of chromatin—the complex of DNA and protein—that are bunched together and closer in three-dimensional space,in compact shape.

2. Transcription factors need to find specific DNA sequences to regulate genes. TADs help solve this search problem by organizing the genome, preventing the "tangled mess" that would otherwise hinder the movement of biological machinery like RNA polymerase.

3. Research, such as the paper by Dota et al., suggests that "intersegmental jumping" across 3D-proximal segments within TADs significantly speeds up the search process for transcription factors compared to simple diffusion.

4. Optimal Compaction: Theoretical models suggest an optimal compaction parameter (gamma) for these domains, around 0.7. Empirical measurements of approximately 8,000 human TADs show that they align closely with this theoretical optimum, rather than being too collapsed or too open.

5)Evolutionary Dilemma: The panel noted that the formation of TADs requires specific code (a 19-nucleotide sequence), the CTCF protein, and cohesin rings driven by ATP hydrolysis. They argue that this system presents a challenge for undirected evolutionary theories because intermediate, less-optimized states might have been energetically costly or non-functional, offering no survival advantage until the system is nearly perfect. The speakers suggested that TADs are a hallmark of eukaryotic genomes and were likely a necessary evolutionary or design solution to manage the vastly larger genomes of eukaryotic cells.

My argument -

I found it strange. They are looking at complex TADs of mammals which require cohesin and ctcf proteins interaction. They said ( mainly Truman) that this system is irreducibly complex.

The things in actuality , are much different from what they are saying. Many eukaryotes lack the ctcf - cohesin based TADs. So it's reducible . Like nematodes completely deleted their ctcf gene ,they rely on different mechanism of tad formation. Only basal nematodes like Trichinella spiralis have ctcf.

Insects also lack cohesin- ctcf based TADs network as in higher vetebrates. Platyhelminthes also completely lack the ctcf gene ,like more derived nematodes. They are still surviving . Yeasts completely lacks TADs . Plants have TADs but not like that in higher vetebrates. Jellyfish and sponges also lack the vetebrates level cohesin -ctcf mediated TADs organisation.

They are shocked . Why? Bcoz how is it possible for TADs to spread throughout the genome ?

Well it's easy . Start from simple- cohesin is much older than ctcf. Ctcf gene evolved in common ancestor of bilateria. Over time it acquired mutations in its n terminal region ( front part) which acted as binding site for cohesin,hence helping in formation of TADs.

Ctcf binding sites in genome mainly exist in non coding regions of dna . In few exceptions,they can exist in coding regions. Initially in primitive genome only few such binding sites for ctcf protein could have existed. Then n terminal mutations in the gene made the affinity for this protein increase towards cohesin and form partial tad networks ( not complete) But the most important events in the evolution of so many binding sites for ctcf occured due to retrotransposons which carried ctcf binding sites by copy and paste mechanisms. Those organisms in which ctcf disrupted genes by copy and paste mechanisms were removed from the gene pool. Only those survived whose genes and regulatory elements weren't affected by this retrotranspositions. Also they spread by wgd events. Hence more cohesin ctcf interaction leading to more TADs formation.

Here are links of retrotransposition part

https://www.sciencedirect.com/science/article/pii/S0092867411015078

https://www.nature.com/articles/s41467-020-15520-5

Now creationist might ask ,how did not fully cohesin -ctcf tad genome could exist ? At one time in the past there weren't enough ctcf binding sites ,hence limited compaction of dna.

Nope ,other mechanisms of compaction of dna existed. It's just another extra mechanism that organisms benefitted from.

Finally , Truman says evolutionary novelty is a story . You require lots of energy ,dna ,proteins and finally a long time after over generations mutations fine tune a protein .Intermediate steps are detrimental.

This is laughable. Each step will be beneficial. If a gene gets duplicated,let's suppose ,how much energy is required to maintain it? Negligible. A huge amount of atp is required to maintain membrane transporters and other things. Am I correct ?

And James Tour as usual says that junk dna have functions

What do you all think of Truman ? Any more extra information on TADs ??

Btw ,can someone pls tell me that whether primitive systems require the same compaction parameters value as talked about here?

Waiting for all of your response.

Part 1

Hello there , yesterday I posted about a guy named Onsi Fakhouri. Recently he has been coming to Tour's channel along with Stadler and Truman complaining about different things like origin of life and evolution based topics

I am here referencing a video on James Tour's channel titled - Evolution vs design.

I am making a part wise post of the video. They talked about a lot of points.

So I am breaking each point into distinct parts to keep my post short and simple.

Ok ,let's go -

Topic- Fruit Fly Embryo Development & Signaling Networks

Onsi says the following points-

Precise Positional Information (3:52 - 4:14): The embryo successfully differentiates cells based on location along an axis with 1% resolution. He argues that such high-level accuracy is remarkable and essential for the embryo to develop correctly.

Sophisticated Signaling Networks (4:26 - 6:00): This resolution is achieved through a complex, multi-layered processing system involving maternal inputs and four "gap genes." He emphasizes that this is a highly engineered system designed to filter noise and maintain precision.

Quantitative Optimality (10:13 - 13:25): Drawing on the work of physicist Bill Bialek ( a biophysicist) and colleagues, they note that the gene regulatory network is tuned to an optimal state. Modeling suggests that the system requires exactly four genes to hit the 1% resolution target—three are insufficient, and five are unnecessary "overkill."This overkill statement is Onsi's.

The "Knobs" (10:20 - 10:34, 13:42 - 14:14): As explained by him ( Fakhouri) , the model assigns two specific parameters to each of these interaction paths. He says that when you aggregate these variables across the entire regulatory graph defined in the model, you arrive at approximately 56 adjustable "knobs" or parameters.

Physics-Based Modeling (10:20 - 10:34, 13:42 - 14:14): These parameters were identified by Bill Bialek and colleagues as they attempted to build a predictive, quantitative model that could account for how the embryo achieves its 1% positional resolution. The complexity of having to tune all 56 variables simultaneously is a key point in the speakers' argument regarding the difficulty of this system arising through purely undirected evolutionary processes.

The Problem of Evolutionary Tuning (13:42 - 14:14, 58:47 - 59:18): Onsi and his arguments are that with 56 different parameters ("knobs") to adjust, the complexity is so vast that it is mathematically implausible for random mutations and natural selection to have fine-tuned the system to this optimal state without a directed, purposeful cause.

He also says these - Because there are hundreds of nuclei floating in the exact same fluid, they are all competing for the same maternal signaling proteins (like Bicoid). He argues that trying to pass an accurate, uncorrupted chemical message through a chaotic, crowded soup of 100+ nuclei without it getting distorted or lost in molecular noise is mathematically implausible. He uses the "Every Nucleus Knows Its Place" Claim: He points out that despite this chaos, each individual nucleus reads the local concentration of proteins so precisely that it "knows" its exact position along the body axis within a 1% margin of error. He argues that this level of coordinate-mapping across hundreds of independent points simultaneously requires an upfront, engineered communication network.

I was like wth? Why did they pick up a modern gene regulatory network?

Also Truman's words

The Knowledge Problem (14:26 - 15:22): He argues that a random process, such as mutation, lacks the "foresight" to know in advance that specific genes are required for a regulatory network, meaning it must simultaneously avoid disrupting thousands of other genes while attempting to build the correct ones.

And yes ,these are direct words of Truman

What do you all think about this? And Onsi ? He is in a nutshell saying that the entire network is too complicated to have evolved. It's designed. Same old creationist rhetoric. So many parameters. Mutate a gene , and boom something bad is going to happen . Irreducible complexity.

Wanna hear all about your words. Edit - https://www.pnas.org/doi/10.1073/pnas.2402925121 It seems like onsi is talking about this paper.

Hi there , I have been seeing james tour bringing a new guy named Onsi Fakhouri who is claims to be a phd , astronomer and is Pivotal’s Senior Vice President of Cloud R&D since a few days ,to talk about topics on evolution and debunk it . Any opinions on this guy ?

James tour also recently posted a video yesterday with him ,Stadler and Truman Evolution vs Intelligence.