Posted on 02/28/2011 12:05:32 PM PST by SeekAndFind
“Of all the different species that evolved, which ones have the species they evolved from still around? You’d think there would be a lot . . . “
A lot? When over 99% of all species that ever existed are now extinct. How does that “kind of prove your point”?
What IS your point? Dare I ask Mr. ‘why don’t apes evolve into humans’ and expect an intelligent answer? LOL!
So ribosomes with mutations resistant to antibiotics that targeted them existed before the antibiotics? Why, when they don't work as good as ‘wild type’ ribosomes? Why would they exist?
“never been demonstrated” is absolutely incorrect. Mutations to an enzyme that make the new antibiotic (based upon Penicillin) that previously didn't bind, now get bound and metabolized - as well as mutations that lead to the overexpression of said mutated enzyme - HAS been demonstrated. That is why Methocillin, that previously was immune to degradation by penicillinase, now has resistance present in some populations. Through mutation of the penicillinase gene.
So how do you explain why a bacteria would HAVE an error prone DNA polymerase, or why it would be expressed during stress?
What you have just describe does not argue for evolution in the absolute sense, at least NOT evolution as Darwin himself describes it.
So, sorry to say, I have to disagree with you.
Molecular analysis of the genetic events that lead to antibiotic resistance do not necessarily support this common assumption.
Many bacteria become resistant by acquiring genes from plasmids or transposons via horizontal gene transfer.
Horizontal transfer, though, does not account for the origin of resistance genes, only their spread among bacteria.
Mutations, on the other hand, can potentially account for the origin of antibiotic resistance within the bacterial world, but involve mutational processes that are contrary to the predictions of evolution.
Instead, such mutations consistently reduce or eliminate the function of transport proteins or porins, protein binding affinities, enzyme activities, the proton motive force, or regulatory control systems. While such mutations can be regarded as “beneficial,” in that they increase the survival rate of bacteria in the presence of the antibiotic, they involve mutational processes that do not provide a genetic mechanism for common “descent with modification.” Also, some “relative fitness” cost is often associated with such mutations, although reversion mutations may eventually recover most, if not all, of this cost for some bacteria. A true biological cost does occur, however, in the loss of pre-existing cellular systems or functions. Such loss of cellular activity cannot legitimately be offered as a genetic means of demonstrating evolution.
The theory of evolution proposes that all life on Earth had a common origin.
Hence, all life shares a common evolutionary ancestry from which it has descended, i.e., the “common descent” of life. Those are not my ideas, it was DARWIN’s.
In a summarizing statement, Darwin stated that “the theory of descent with modification embraces all the members of the same great class or kingdom ... all animals and plants are descended from some one prototype.”
Therefore, through this overall common “descent with modification,” the theory of evolution claims to account for the origin and diversity of all biological development on Earth. Thus, common “descent with modification” provides a more appropriate and functional definition of the theory of evolution, and this post refers to evolution in this context. This definition also entails several “predictions” regarding the types of genetic change necessary for common evolutionary descent. Such changes must provide more than mere changes in phenotype; they must provide a genetic mechanism that accounts for the origin of cellular functions and activities (i.e., regulatory systems, transport systems, enzyme specificity, protein binding affinity, etc.).
Unfortunately (as I look at how things are described ), Genetic changes that reduce or eliminate any of these cellular systems provide NO GENETIC MECHANISM for common “descent with modification.”
Rather, such changes are actually the antithesis of this descent, reducing or eliminating a pre-existing system of biological complexity (a reversal of “descent with modification”). Therefore, these genetic changes offer no example of a genetic mechanism for the “evolutionary” acquisition of flight by non-flying organisms, cognition by non-cognitive organisms, photosynthesis by non-photosynthesizing organisms, etc.
Yet the theory of evolution requires such events to have occurred, and requires mutations capable of such genetic changes. Hence, the predictions of evolution require specific types of changes, not just so-called “beneficial” mutations. Therefore, despite the great claims that have been made, it is imperative to question whether acquisition of antibiotic resistance is a valid example of evolutionary change that supports the predictions of the evolutionary theory (i.e., the theory of common “descent with modification”).
We do know however that one means by which bacteria can acquire antibiotic resistance is via the horizontal transfer of antibiotic resistant genes. Such transfer of resistance genes is common , accounting for many examples of resistant bacteria.
But, horizontal transfer merely involves the transfer of resistance genes already present in the bacterial world.
While horizontal acquisition of resistant genes is “beneficial” to those bacteria exposed to a given antibiotic, such gene transfer does not account for the origin or the diverse variety of these genes. As such, it fails to provide a genetic mechanism for the origin of any antibiotic resistance genes in the biological world. Evolution, through the process of common “descent with modification,” predicts it can account for the origin and diversity of life on earth; however, the mere shuffling of pre-existing genes between organisms via gene transfer does not provide the necessary genetic mechanism to satisfy this prediction.
Nor can it readily account for the simultaneous development of both the antibiotic biosynthesis and resistance genes—an evolutionary enigma.
So, sorry to say, horizontal transfer of resistant genes cannot be offered as an appropriate example of “evolution in a Petri dish.”
Regarding your question at the end of your post -— I am not afraid to say I DON’T KNOW other Let’s let the science play out eventually before jumping into an absolute conclusion.
Suffice it to say that I stand by my stance -— IT IS NOT NECESSARY TO TEACH DARWINIAN EVOLUTION IN SCHOOL FOR BIOLOGY TO BE TAUGHT.
You know my point but choose to insult me instead of answering politely.
Thanks.
RE: That is why Methocillin, that previously was immune to degradation by penicillinase, now has resistance present in some populations. Through mutation of the penicillinase gene.
Well, we’re back to the original question...you talk about an ability to survive…penicillin, methicillin, and cephalosporins, etc.
But what about the observation that the gene that confers antibiotic resistance typically resides on plasmids, which are free-floating loops of DNA that were manufactured by other bacteria and released?
For instance, Regular old methicillin-resistant Staphylococcus aureus is not normally harmful, but when a single bacterium acquired the methicillin-resistant plasmid from its immediate environment, it and its descendants became more fit to survive in the antibiotic-laden environment of hospitals.
Here unfortunately, I see the typical EQUIVOCATION.
Evolution is described in textbooks as the way that nature manufactures new genetic information from nothing. However, when this bacteria “evolved,” NO NEW INFORMATION was generated.
Rather, old information from an old plasmid was acquired by the bacteria, which used its well-designed DNA acquisition machinery (sorry for the term, I know you don’t like the word design, you can substitute another word for it if you wish, maybe — pre-existing DNA ? ).
So, why is it not euqally reasonable to conclude that this bacteria is built-in (ooops, sorry for that word) to survive well?
So how did bacteria acquire the ability to bind and metabolize (and thus render harmless) Methocillin?
Through mutation of the Penicillinase gene. Obviously.
Why did this mutation persist in the population?
Through natural selection of genetic variation. Obviously.
So why would bacteria HAVE an error prone DNA polymerase and why would it be expressed during times of stress?
hey...no stereotyping. !!
blacks get sunburned. they aren’t immune from melanoma.
these guys must be smoking wacky weed.
RE: The “information” on how to bind Methocillin with Penicilinninase was NOT acquired from horizontal gene transfer. How could it be when there was no Methocillin in the environment and Methocillin was specifically designed to NOT be bound by Penicillinase.
Methicillin-resistant Staphylococcus aureus (MRSA) is just the most recent in a long line of bacteria that has shown evidence of resistance to antibiotics that previously was clearly susceptible to a certain antimicrobial agents.
AS I scan the literature, I find out that there are numerous mechanisms, e.g. loss of enzymatic activity can result in metronidazole resistance, mutations associated with antibiotic resistance involve the loss or reduction of a pre-existing cellular function/activity, i.e., the target molecule lost an affinity for the antibiotic, the antibiotic transport system was reduced or eliminated, a regulatory system or enzyme activity was reduced or eliminated, etc. and several bacteria, including Escherichia coli, construct a multiple-antibiotic-resistance (MAR) efflux pump that provides the bacterium with resistance to multiple types of antibiotics, including erythromycin, tetracycline, ampicillin, and nalidixic acid are just a couple of them.
Understanding that there are multiple reasons for bacterial resistance to antibiotics ought to help us to see this ability as the result of a complex and often diverse interactions rather than a simple and straightforward ability of organisms to change over time.
I don’t think that bacterial resistance to antibiotics does anything to SUBSTANTIALLY CHANGE the core components of bacteria. As with all other mutations, information is being LOST or ALTERED in some way.
NO NEW INFORMATION is being transmitted and this is a BASIC REQUIREMENT for the types of changes predicted by Darwinian evolution.
Single cell bacterial remain single cell bacteria.
These mutations also cannot provide a mechanism that continues to “evolve” the level of protein specificity or protein activity that is necessary for normal cellular function.
So what are they ?
Such mutations are excellent examples of bacterial ADAPTATION. THAT’s AS FAR AS I’LL GO FOR NOW.
Yet, these are the very examples evolutionists offer as verifiable demonstrations of “evolutionary change.” Ironically, these mutations are, in fact, verifiable examples of an existing complex entity being mutated to a level of greater simplicity.
SO yes, Antibiotic resistance is certainly an example of change, but to call it Darwinian evolution is stretching it (bacteria remain bacteria).
Lol! Yes, they can get skin cancer, but I have noticed that older people who are black have very few wrinkles. (SIGH)
Survival during treatment with an antibiotic is a substantial change that allows pathogenicity instead of eradication.
The ONLY way to explain how a bacterial population could develop antibacterial resistance through mutation, and why such mutations (or those gained via horizontal gene transfer) would be selected for as long as the antibiotic was in use.
There IS NO OTHER SCIENTIFIC EXPLANATION.
The only way to describe how bacteria gain antibiotic resistance and how it accumulates and persists within a population is the theory of natural selection of genetic variation.
There is no need for the bacteria to speciate or to change into something else for it to be the mechanism.
Your argument is as delusional as saying that unless a Planet or Sun formed, gravity didn't take place - because gravity explains how Planets and Suns form - so unless a Planet or Sun formed - it wasn't gravity.
Speciation is not necessary for evolutionary change to take place.
For example, changes in skin color did not make human populations into different species - yet evolution through natural selection of genetic variation is the only scientific mechanism that explains it.
“Speciation is not necessary for evolutionary change to take place.”
I don’t think anyone really has a problem that bacteria might mutate and in so doing achieve a level of resistance. If this is evolution, then we are all evolutionists. You win the semantics battle but do not win many minds over to believe that this mechanism can account for whole new complicated structures and functionalities. I have read somewhere (other than Seek and Find’s posts) that when a bacteria develops resistance through mutation, the gene that mutates really suffers regarding the function it serves to the cell. The bacteria survives but is less robust and contains no new information that puts the bacteria on the road to more complexity. Hence, bacterial mutation to allow survival cannot be used as an example of descent with modification.
So is skin color change.
So is digesting nylon.
So is any number of morphological traits.
Brought about by natural selection of genetic variation, including variation brought about via mutation.
In bacteria they have an error prone DNA polymerase that they express during stress instead of the high fidelity one. This increases variation.
That is why novel antibiotics that formerly always worked will always give rise to antibiotic resistance.
Because of evolution through natural selection of genetic variation.
Check the link on the e. coli that digest citric acid. That is a new function. So is digesting nylon in the bacteria outside nylon factories.
Bacterial mutation that allows survival through selection of genetic variation IS an example of descent with modification.
The fact that DNA is the molecule of heredity and even high fidelity DNA polymerase cannot copy it exactly means that descent with modification is inevitable.
There’s a saying, “black don’t crack.”
I’ve always been curious about body hair and why that differs among ethnic groups.
Genesis 2 does not describe an "eighth" day of creation. Genesis 1 and Genesis 2 describe the same creation event, but whereas Genesis 1 is general and speaks in terms of categories (man, waters, etc.) Genesis 2 is specific and speaks within those categories (Adam, Tigris/Euphrates etc.)
But if that's not enough to convince you, consider the logic of the proposition that on day 8 there was not a man to till the ground, yet, we know man was already created on day 6.
This notion, that there are two different creation stories in Genesis is nonsense.
Then who did Cain go to Nod and live with? Did He marry his sister? We are all one family through THE Adam, who was the progenitor of David and Yeshua on Earth. If you cannot open your mind to something that explains a lot of the inconsistencies of Scripture, it is your loss. If you believe that Adam and Eve were the first two human beings created, and all people came from them, how do you reconcile that they must have had their children marry each other, then their grandchildren, their great grandchildren.
RE: Bacteria need not become anything other than bacteria to exhibit evolution through natural selection of genetic variation, yet you seem fixated upon the delusion that it does.
Well then, we are simply using the term “evolution” in different ways. I see it as adaptation with its environment, with little siginifcant change, you seem to see it differently and then call people who disagree delusional ( is this the way you discuss things? This habit of yours seem to permeate this thread with other posters as well ).
But then of course we disagree.
If you simply suggest an awareness of on-going changes in pathogenic bacteria, I would concur. Bacteria do acquire resistance quickly, and many older drugs no longer work in hospitals and clinics.
But then I don’t see how this observation per se makes for instance, a Darwin Sceptic different from a Darwinian. Both are interested in finding new drugs that will work and seek to heal the sick.
A conclusion made by many scientists in experiments is that acquiring antibiotic resistance through mutation or horizontal transfer is “costly.” There is a tradeoff: for survival in a clinical environment (i.e., antibiotics prevalent), there is a metabolic cost in terms of slower growth. This is called antagonistic pleiotropy.
Antagonistic pleiotropy refers to the genetic expression of multiple competing effects, some beneficial, but others harmful to the organism. It often involves a case where reproduction and viability counter each other in biological fitness.
The gene provides a benefit in one circumstance, but has cost in another.
Don’t get me wrong, the results of various experiments do show that bacteria can change quickly. But although the we have acquisition of antibiotic resistance, I am not sure if we can call it Darwinian evolution.
All it does is demonstrate that bacteria were endowed to change and adapt very quickly in an almost constantly changing environment.
Bacteria have tremendous variability, yet there are limits to such change: the continuity, stability, and reliability of such bacteria are well known.
I mentioned antagonistic pleotropy earlier in the thread.
There is indeed “No such thing as a free lunch”.
A ribosome is a highly specialized structure, and it is the best darn ribosome it can be in a bacteria - and any variation from the theme gets eliminated from the population rapidly.
Until....
Humans make a antibiotic that targets ribosomes. Suddenly variations that don't perform as well at turning mRNAs into functional proteins but ARE resistant to the antibiotic are favored in the population.
LESSON: genetic variation arises in a population as a consequence of imperfect replication (or controlled expression of error prone DNA polymerase), most variations are, absent a change in the environment, detrimental and eliminated. Changes that meet a need in a changed environment that caused stress (an antibiotic that attacks ribosomes) are retained in the population through natural selection of genetic variation.
Cease being uncertain that you could call that evolution through the theory of natural selection of genetic variation, because it is exactly the mechanism that Darwin described.
http://www.answersingenesis.org/articles/nab/are-there-different-races
Skin colors are mentioned more towards the end of this article.
Ignoring their incorrect recitation of what evolution actually entails, when you get to the “explanation” for skin color differences they say it is mutation and selective pressure.
Mutation and selective pressure upon that genetic variation.
The exact mechanism of evolution that Darwin described.
So apparently ‘answers in genesis’ agrees with modern science that mutation created variation and selective pressure upon that variation is responsible for differences among human populations.
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