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Icons of Evolution

Gene2memE

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Stephen W. Schaeffer (Professor Emeritus of Biology) claims that the theory of common descent has proven useful in identifying so-called conserved sequences in human DNA (if "conserved", such sequences are understood to serve a functional purpose ... as opposed to so-called junk DNA, which is generally understood to serve no functional purpose).

My understanding is that process involves comparing human and chimps DNA, then finding similar DNA sequences, which are alleged (according to the theory of common descent) to have been "conserved" by natural selection from a common ancestor.

But it seems debatable to me if identifying conserved sequences has actually proven fruitful in curing or improving the treatment of any disease.

Conserved sequences aren't just compared with chimpanzees and other primates, we see them in comparisons throughout the rest of life. Here's a paper comparing the genomes of humans and pufferfish, which found "nearly 1,400 highly conserved non-coding sequences".


What's really cool is that despite last sharing a common ancestor about 450 million years ago, the comparison found that: "Without exception, all reported examples of non-coding conservation between these two species have been associated with genes that play critical roles in development." Which suggests that purifying negative selection is at play here (and has been for a very, very long time).

Here's another paper that shows humans have around 500 'ultraconserved' elements in common with the rat and mouse genomes. Ultraconserved meaning regions of at least 200 contiguous nucleotides that are perfectly conserved between the genomes.


What's fascinating is that there are still lots of unanswered questions about these 'ultraconserved' regions. We know that a majority of these regions play critical roles in regulating gene expression that is responsible for the development/growth of an organism - yet, when deleted half of them don't actually seem to have no impact on an organism's "viability, fertility, or fecundity". Why?
 
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Buzzard3

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Conserved sequences aren't just compared with chimpanzees and other primates, we see them in comparisons throughout the rest of life. Here's a paper comparing the genomes of humans and pufferfish, which found "nearly 1,400 highly conserved non-coding sequences".


What's really cool is that despite last sharing a common ancestor about 450 million years ago, the comparison found that: "Without exception, all reported examples of non-coding conservation between these two species have been associated with genes that play critical roles in development." Which suggests that purifying negative selection is at play here (and has been for a very, very long time).

Here's another paper that shows humans have around 500 'ultraconserved' elements in common with the rat and mouse genomes. Ultraconserved meaning regions of at least 200 contiguous nucleotides that are perfectly conserved between the genomes.


What's fascinating is that there are still lots of unanswered questions about these 'ultraconserved' regions. We know that a majority of these regions play critical roles in regulating gene expression that is responsible for the development/growth of an organism - yet, when deleted half of them don't actually seem to have no impact on an organism's "viability, fertility, or fecundity". Why?
Interesting indeed.

My knowledge of genetics is very (very) limited, but it seems to me that the concept of conserved sequences is predicated on the assumption that some DNA is considered functionally useless - aka "junk" DNA.

It also seems to me that if a function cannot be ascertained for some DNA sequences, it is regarded as non-functional. If so, surely the possibility exists that at some later date, when knowledge of genetics has advanced, it could be discovered that "junk" DNA is in fact functional, thus throwing the concept of conserved sequences into serious doubt.
 
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Warden_of_the_Storm

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If no one is aware of any use for the theory of common descent in medical or biological research, it's a fair guess that none exist.

You just saying that no-one is aware of any use for the theory of common descent in medical or biological research does not mean that no-one is aware.

You keep doing this: just saying that something is wrong and doing nothing to show that something is wrong, especially with regards to common descent since, oh surprise surprise, WE HAVE EVIDENCE.
 
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AV1611VET

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You just saying that no-one is aware of any use for the theory of common descent in medical or biological research does not mean that no-one is aware.

If we're so closely related to Magilla Gorilla, then why can't we receive organ transplants from them?

We can't even receive organ transplants from each other without requiring anti-rejection medication for the rest of our lives.
 
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Warden_of_the_Storm

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If we're so closely related to Magilla Gorilla, then why can't we receive organ transplants from them?

We can't even receive organ transplants from each other without requiring anti-rejection medication for the rest of our lives.

Yeah, I'm not asking you AV. So sling your hook.
 
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River Jordan

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sfs

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My argument is that the theory of common descent (that all life on earth descended from a common ancestor - often referred to as the theory of evolution) is useless in the field of medical science.
Your argument is wrong. Common descent is routinely used in biomedical research. As others have pointed out, conserved non-coding regions discovered through comparative genomics (and not just between humans and chimps) have been highly useful in identifying regulatory regions, which in turn are critical for untangling the complex web of molecular interactions that occur in cells.

Comparative genomics also allows us to identify the ancestral allele at variable sites in the genome, which is quite useful for detecting parts of the genome that have been under recent positive selection. It even allows us to identify high and low mutation rate regions of the genome, which can also be useful for various reasons.
 
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Buzzard3

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Your argument is wrong. Common descent is routinely used in biomedical research. As others have pointed out, conserved non-coding regions discovered through comparative genomics (and not just between humans and chimps) have been highly useful in identifying regulatory regions, which in turn are critical for untangling the complex web of molecular interactions that occur in cells.

Comparative genomics also allows us to identify the ancestral allele at variable sites in the genome, which is quite useful for detecting parts of the genome that have been under recent positive selection. It even allows us to identify high and low mutation rate regions of the genome, which can also be useful for various reasons.
Fair enough. Thank you for the information. That's very interesting.
 
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DennisF

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The development of new antibiotics to combat the evolution of resistant strains of bacteria provides an excellent example of the application of the theory of evolution.

AspectEvolutionary PrincipleHow Pathogens Use It to Evolve ResistanceSpecific Ancestor ExampleHow Medicine Uses Evolution to Counter Resistance
MutationRandom genetic change introduces variationSpontaneous mutations in bacterial genes confer resistance (e.g., rpsL)Mycobacterium tuberculosis H37Rv (pre-streptomycin)Screen for naturally occurring bacterial compounds (e.g., streptomycin); use mutagenesis to find weak spots in bacteria
Natural SelectionFitter variants survive and reproduceDrug-resistant strains survive treatment and dominateStaphylococcus aureus 8325-4 (pre-penicillin resistance)Use high-throughput evolution models to simulate resistance and pre-select drugs less likely to fail
Variation within PopulationsGenetic diversity affects survival outcomesResistant subpopulations survive while others dieMycobacterium tuberculosis wild strains (mixed katG variants)Tailor combination therapy (e.g., rifampin + isoniazid) to minimize survival of diverse resistant clones
AdaptationPopulations evolve to changing environmentsEnterococcus faecium evolves vancomycin resistance via vanA genesE. faecium DO (vancomycin-sensitive)Develop next-generation antibiotics targeting new pathways (e.g., linezolid targeting protein synthesis)
Survival of the FittestMost fit reproduce in the new environmentMDR strains outcompete sensitive ones in drug-rich environmentsKlebsiella pneumoniae ATCC 13883Rotate or cycle antibiotics in hospitals to reduce selective pressure on any one resistance trait
Selective PressureEnvironmental conditions shape evolutionAntibiotic overuse selects resistant bacteriaE. coli K-12 (pre-fluoroquinolone resistance)Use antimicrobial stewardship to reduce unnecessary pressure; limit broad-spectrum drug use
Co-evolutionInteracting species evolve in responseBacteria develop β-lactamases, we develop β-lactamase inhibitorsH. influenzae Rd KW20 (non–β-lactamase producer)Design inhibitors (e.g., clavulanic acid) based on enzyme evolution structure modeling
Evolutionary Arms RaceOngoing adaptations between rivalsPathogens modify surface proteins to evade immunityBordetella pertussis Tohama IContinuously update vaccine components (e.g., DTaP formulation changes) to match new variants
Genetic Drift / Gene FlowRandom changes & horizontal gene transferResistance genes spread across species (e.g., CTX-M plasmids)E. coli K-12 & Klebsiella MGH 78578 (pre-ESBL)Use genomic surveillance to monitor plasmid transmission and inform targeted antibiotic policies
Predictive Power of EvolutionEvolutionary models can forecast changeStreptococcus pneumoniae shifts to non-vaccine serotypesS. pneumoniae D39 (serotype 2)Predict future mutations and preemptively design mRNA or conjugate vaccines (e.g., PCV13, mRNA COVID-19 updates)
This is what some call microevolution and nobody debates it. The real issue is macroevolution - whether major changes in organisms can occur through the proposed mechanisms of neo-darwinian theory. That is the issue. Both sides of this issue have been debated at length at asa3.org the American Scientific Affiliation, a fellowship of Christians in the sciences. So although there is nothing wrong with your assertions about single-celled life evolving, that is not the issue anybody disagrees with.
 
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Hans Blaster

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This is what some call microevolution and nobody debates it.
"microevolution" is just evolutionary change that is so small that creationists can pretend they are OK with it.
The real issue is macroevolution - whether major changes in organisms can occur through the proposed mechanisms of neo-darwinian theory. That is the issue.
"macroevolution" is just a redefinition of the evolutionary changes creationists have had a problem with for decades. They aren't special.
Both sides of this issue have been debated at length at asa3.org the American Scientific Affiliation, a fellowship of Christians in the sciences.
:rolleyes:
So although there is nothing wrong with your assertions about single-celled life evolving, that is not the issue anybody disagrees with.
I doubt that.
 
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DennisF

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"microevolution" is just evolutionary change that is so small that creationists can pretend they are OK with it.
That's a rather broad sweep. Some creationists are also supportive of neo-darwinian theory.
"macroevolution" is just a redefinition of the evolutionary changes creationists have had a problem with for decades. They aren't special.
Egad, if you know anything from science you know that nonlinear systems are modeled at a given point - an operating-point - in their nonlinear functions and that incremental changes around that point are how they are linearized so that linear systems theory can be applied to describe their behavior around that point. Physicists call it perturbation theory. Electronics engineers call it small-signal or incremental modeling. This not only applies to transistors but also to evolutionary development.

(The Santa Fe Institute has put plenty of work into this. Have you even heard of them?)

As the extrapolation of differentials from the op-pt increases, the validity of the model diminishes. Once the evolutionary changes being considered are too large, the bacteria-level model no longer has validity.
 
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sjastro

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This is what some call microevolution and nobody debates it. The real issue is macroevolution - whether major changes in organisms can occur through the proposed mechanisms of neo-darwinian theory. That is the issue. Both sides of this issue have been debated at length at asa3.org the American Scientific Affiliation, a fellowship of Christians in the sciences. So although there is nothing wrong with your assertions about single-celled life evolving, that is not the issue anybody disagrees with.
The left hand column of the table you quoted defines the drivers for both macro and microevolution. Macroevolution is the accumulation of microevolution events over geological timescales which is the mainstream view of evolution.

My response was to a creationist who probably gets his information from creationist sites such as AIG and ICR not the American Scientific Affiliation.
AIG and ICR are renowned for their dishonest portrayals of mainstream science, the subjects of macro and microevolution are no exception, their rejection of the connection between the two is not based on any science but on the false dichotomy that no connection automatically validates creationism.

DennisF:

Egad, if you know anything from science you know that nonlinear systems are modeled at a given point - an operating-point - in their nonlinear functions and that incremental changes around that point are how they are linearized so that linear systems theory can be applied to describe their behavior around that point. Physicists call it perturbation theory. Electronics engineers call it small-signal or incremental modeling. This not only applies to transistors but also to evolutionary development.

(The Santa Fe Institute has put plenty of work into this. Have you even heard of them?)

As the extrapolation of differentials from the op-pt increases, the validity of the model diminishes. Once the evolutionary changes being considered are too large, the bacteria-level model no longer has validity.
With regards to your response to @Hans Blaster, Hans happens to be a physicist and your transistor analogy has a fundamental problem as to have a perturbation you need a fixed or equilibrium starting point around which perturbation occurs. While this is not a problem with transistors, there are no fixed or equilibrium points in evolution as the starting point for evolution namely mutations are by their very nature random.

While the Santa Fe Institute does challenge the mainstream view of the connection between macroevolution and microevolution it is not an endorsement for creationism and provides an alternate hypothesis at bacterial levels where bacteria are modelled as large population networks. It however does not refute the mainstream model at bacterial levels.

AspectMainstream Evolutionary BiologySanta Fe Institute (Complex Systems Approach)
Core ModelPopulation genetics: allele frequency changes under selection, drift, mutation, and gene flowComplex adaptive systems: interaction networks, feedback, emergent properties
Mutation RoleRandom mutations drive variation; modeled with fixation probabilitiesMutations interact with dynamic systems; may trigger emergent behaviors
SelectionActs on genetic variants within a fixed environmentActs within a co-evolving, possibly shifting environment (e.g., phages, hosts)
AdaptationGradual changes in traits based on fitness advantagesNonlinear adaptation through system-level restructuring and feedback
Horizontal Gene Transfer (HGT)Treated as an exception or special caseCentral mechanism for network rewiring and innovation
Biofilms / CommunitiesOften modeled as individual strains in competitionViewed as distributed, interactive systems with emergent cooperation or specialization
Modeling ToolsWright-Fisher models, mutation-selection balance, molecular evolution theoryFitness landscapes (e.g., NK models), agent-based models, network theory
Innovation (e.g., antibiotic resistance)Stepwise accumulation of beneficial mutations, or plasmid acquisitionInnovation emerges from modularity, recombination, and network plasticity
Fitness LandscapesFixed or slowly changing; individuals climb fitness peaks over timeRugged, dynamic landscapes; organisms may explore, jump, or be driven across valleys
Equilibrium ViewPopulations may stabilize under selective pressuresSystems are dynamic, far-from-equilibrium, with ongoing restructuring
 
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Hans Blaster

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That's a rather broad sweep. Some creationists are also supportive of neo-darwinian theory.
LOL. What creationist support any Darwinian theory, neo, or alt? The only creationists that have "supported" evolution of any form are the YECers who need some sort of hyperevolution to turn their ark "kinds" into multiple species.
Egad, if you know anything from science you know that nonlinear systems are modeled at a given point - an operating-point - in their nonlinear functions and that incremental changes around that point are how they are linearized so that linear systems theory can be applied to describe their behavior around that point.
Who hasn't linearized a set of coupled, non-linear PDEs and solved them for billions of degrees of freedom?
Physicists call it perturbation theory.
Some areas of physics use that terminology, like QFT.
Electronics engineers call it small-signal or incremental modeling. This not only applies to transistors but also to evolutionary development.

I've seen the evolutionary theorists throw up a few simple systems of equations from time to time, but what does any of this have to do with the so-called "macro-evolution"?

(The Santa Fe Institute has put plenty of work into this. Have you even heard of them?)
I've heard of them, but never seen any of their work in the literature. Was it on engineering electronics? (I don't read engineering.)
As the extrapolation of differentials from the op-pt increases, the validity of the model diminishes. Once the evolutionary changes being considered are too large, the bacteria-level model no longer has validity.
Again, you seem to think "macro evolution" is some sort of differential equation. I don't think you comprehend biology that well either.
 
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DennisF

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The left hand column of the table you quoted defines the drivers for both macro and microevolution. Macroevolution is the accumulation of microevolution events over geological timescales which is the mainstream view of evolution.
I didn't quote from a table in my response. I agree that "Macroevolution is the accumulation of microevolution events over geological timescales" is a mainstream view among evolutionary biologists, but that is the crux of the issue in the creation-evolution debate. The SFI recognizes that there are interesting large-scale possibilities that are not incremental in how life could have developed.

Because the origin of life, especially human life, is such a basic question for us as humans, it encompasses the domain of worldviews or religion, defined as the organized observance of a worldview - hence the debate that brings God, Genesis and the biblical and other worldviews into the discussion. For some, the scientific and theological aspects of the issue can be related by realizing that no matter how it occurred and what scientific explanation is ultimately given it, that is how the Creator brought it about.

The real opponents are the idea that the present physical world is purposive and the product of an intelligence on one side versus what essentially reduces to nihilsm on the other side - the view that nothing is ultimately of significance because everything is accidental. Purpose versus accident is a debate conducted behind the facade of science vs religion.
My response was to a creationist who probably gets his information from creationist sites such as AIG and ICR not the American Scientific Affiliation.
AIG and ICR are renowned for their dishonest portrayals of mainstream science, the subjects of macro and microevolution are no exception, their rejection of the connection between the two is not based on any science but on the false dichotomy that no connection automatically validates creationism.
It is not really linguistically honest to refer specifically to the YEC position as "creationism" when anyone who holds a biblical (or for that matter, Vedic Hindu) worldview also has a creationist view of origins. And some of these people have no real conflict with neo-darwinian evolutionary theory.
With regards to your response to @Hans Blaster, Hans happens to be a physicist and your transistor analogy has a fundamental problem as to have a perturbation you need a fixed or equilibrium starting point around which perturbation occurs. While this is not a problem with transistors, there are no fixed or equilibrium points in evolution as the starting point for evolution namely mutations are by their very nature random.
The word random comes from probability theory and means that there is no prior information that would prefer one outcome over another. Consequently, because the causes for mutations (or whatever drives evolution) are not known, evolution is studied probabilistically, not causally. (SFI is trying to move closer to causality.) That is sometimes criticized by anti-evolutionists, but much of science involves probabilistic reasoning, even in control in engineering, and nobody attacks its use there.

Perhaps I could have made the case better for the difference between incremental and large-signal or total-variable analysis; they are clearly quite different, and that is in part what drives work like that of the SFI and also induces YECers to attack biological evolution generally. ("From fish to Gish", as Dwayne Gish put it.) The key issue is whether the present level of complexity of life can unfold without intelligent input to guide it. That is the issue between evolutionary creationists (ECers) and Intelligent Design advocates (IDers). No conclusive answers have been given to the better arguments of the IDers, from the ECers or anyone else. That is why the issue persists. The SFI work is interesting in this context because some of it explores this very issue. Even Richard Dawkins has his doubts when he says that life appears as though it were designed. The "as though" is purely a consequence of his presuppositions. The evidence that he observes is that it is designed. (I once wrote a paper on "Design in Nature and the Nature of Design".)

Perhaps in several decades, if not centuries, we will know enough to properly address these contentious issues! The key to success in research is in knowing how to address the right questions.
While the Santa Fe Institute does challenge the mainstream view of the connection between macroevolution and microevolution it is not an endorsement for creationism and provides an alternate hypothesis at bacterial levels where bacteria are modelled as large population networks. It however does not refute the mainstream model at bacterial levels.
- at the bacterial levels. This is microevolution at an incremental level. We know life has malleability at this simpler level of complexity. How far up the chain of complexity can this be taken? That is an interesting question, one that the SFI people recognize.
 
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sfs

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LOL. What creationist support any Darwinian theory, neo, or alt?
Theodosius Dobzhansky, for one. From his famous article, "Nothing in Biology Makes Sense Except in the Light of Evolution": "It is wrong to hold creation and evolution as mutually exclusive alternatives. I am a creationist and an evolutionist." There's also a recent movement to rebrand theistic evolution as 'evolutionary creationism'. In both cases, they're swimming upstream against the common usage of creationist to denote a theistic opponent of evolution.
 
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sfs

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No conclusive answers have been given to the better arguments of the IDers, from the ECers or anyone else. That is why the issue persists.
What are these better arguments? All of the ones I've seen have been pretty bad. (And of course, lots of issues continue to persist despite conclusive answers -- ask any flat-earther or young-earth creationist.)
 
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