How can you demonstrate E.coli doesn’t have a built in mechanism?
No ifs or buts. It only spreads temporarily in controlled environments. How can you not see that all these are controlled environments? Same with black death, the influenza outbreak, pesticide resistance, etc. They all died out before taking over the Universe. Nonlinearity and negative feedback at work.
You default to telling stories, which is fine, but not science.
Interesting, but no need to feel superior for this bit of info. This safety/consistency measure adds nothing to the argument. People have bred dogs, etc. for ever, and now E.coli. Question is: without presupposing evolution, can you demonstrate this E.coli change is not a built in mechanism? No, you cannot.
Your “superiority” is boring and misplaced when all your arguments are 100% circular logic - presupposing evolution to demonstrate evolution.
Adaptive does not invalidate built-in. Of course built-in mechanisms have to be adaptive to work.[quote=“gbrooks9, post:227, topic:35830”]
Who said anything about Evolution from “bacteria to humans”?
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“The origin of species” - read it.
You keep claiming that the development of antibiotic resistance is a built-in mechanism in e coli rather than the result of mutations / favorable alleles passed on to succeeding generations. A lot is known about e coli, so you should be able to identify that mechanism. What is it and how does it work?
Let’s go back to the development of antibody-producing genes in B cells and the T-cell receptor genes – the DNA manipulation that occurs there occurs in virtually every single individual’s B and T cell precursors. In addition, this occurs only in very specific parts of the genome. The DNA rearrangement that allows the new activity of the citrate transports is the exception, not the rule. Instead of occurring in virtually EVERY organism, it occurred in virtually NONE of the organisms. But changes like this only have to occur in one organism for this mutation to now be present in all the progeny of this organism.
All I can say is “no one has found a similar mechanism in E. coli”, but this is similar to saying “How can you prove Bigfoot doesn’t exist” as proof of his (or her) existence!
Why has your definition of a “controlled environment” made this monumental leap from “hospital setting” to “entire universe”? I’m beginning to understand what you are saying despite the fact that your definitions are changing mid-conversation – God’s creataion has the ability for counter-balancing. Black Death wiped out roughly half of the European population, so I wouldn’t really call that a controlled environment, but it did eventually run its course. Flu outbreaks also run their course. Assuming that antibiotic resistance and pesticide resistance will just go away on their own may be over-optimistic. Even for “routine” bacterial infections, the dosage of antibiotics has had to increase dramatically over the decades – even in bacteria not normally considered “antibiotic-resistant”.
Regardless, I’m still failing to understand how this relates back to your assumption that any of this casts doubt on the theory of evolution.
You’re projecting. You’re the one who falsely accused Lenski of not starting with a single cell. This is a fact that is easily obtained, but you didn’t bother to read the most basic methods before rushing to judgment.
You’re the one claiming superiority in that you understand biology better then the biologists who do biology, remember?
What on earth are you talking about? Are you saying that contagion cannot wipe out a species? Where did you get that idea? The Tasmanian Devil is almost extinct due to a cancer that exploits the T. Devil’s odd social behavior. But there are more systematic discussions of the evidence:
Abstract
“Infectious disease, especially virulent infectious disease, is commonly regarded as a cause of fluctuation or decline in biological populations. However, it is not generally considered as a primary factor in causing the actual endangerment or extinction of species. We review here the known historical examples in which disease has, or has been assumed to have had, a major deleterious impact on animal species, including extinction, and highlight some recent cases in which disease is the chief suspect in causing the outright endangerment of particular species. We conclude that the role of disease in historical extinctions at the population or species level may have been underestimated. Recent methodological breakthroughs may lead to a better understanding of the past and present roles of infectious disease in influencing population fitness and other parameters.”
[Invertebrates]
“One case that was not missed was the loss of the last members of Partula turgida, a snail from French Polynesia that succumbed to an infection of the microsporidian Steinhausia sp. [31]. Steinhausia is a known parasite of various taxa of bivalve molluscans, infecting oocytes and thereby reducing fecundity …”
[Birds]
“Smith et al. [4] identified 18 examples of bird extinctions and extirpations that have been attributed at least partly to infectious diseases. Of these, 16 cases concern endemics that lived in the Hawaiian Islands; most were from one tribe of finches, the Hawaiian honeycreepers (Drepanidini, Fringillidae).”
[Mammals/Rodents]
"the disappearance of two endemic murid species on Christmas Island (Indian Ocean) at the beginning of the 20th century. That the Christmas Island extinctions could be usefully studied at all is due in large measure to the work of the biologist Andrews [47] and, later, the parasitologist Durham [48], both of whom spent considerable time on the island and recorded many valuable observations on the rats before and during their disappearance. "
[General Conclusions]
“Although host-pathogen interactions have been a subject of interest in conservation biology for some time, the possibility that disease might actually drive extinctions in certain contexts has rarely been considered. This is partly due to a general lack of knowledge concerning wildlife pathogens and their microbiology, but it also stems from a lack of well-researched and unequivocal examples of disease-induced loss of naturally occurring populations or species. We anticipate that, with the advent of endeavors such as the Human Microbiome Project [68] and the further development of next-generation sequencing, we will have an increasingly better understanding of microbiological processes in wildlife. Because of their relevance to human health, bat and rodent viromes are being explored with special intensity using high-throughput approaches, with the result that many novel—and potentially significantly pathogenic—viral strains have been identified in recent years …”
It’s pretty hard to prove a negative. I can’t prove invisible car key gnomes don’t hide my car keys in sofa cushions. However, we can assess whether the phenomena we see is consistent with known, studied mechanisms (vs a directed mechanism). For example, we know that DNA polymerase and DNA repair mechanisms have a certain level of fidelity. We can see if the mutations that produce a given form of antibiotic resistance occur at comparable rates.
Also, we can test whether such mutations arise via a special, specific, directed mechanism in response to the environment or whether they occur spontaneously at similar rates in a population not exposed to say, an environment with a particular antibiotic.
Both of these approaches have been considered in examining how streptomycin resistance may be acquired via mutations in the bacterial chromosome. Google ‘spontaneous streptomycin resistance’ for some relevant papers. At least one paper dates back to 1949 and was an extension of the Luria–Delbrück technique.
There is solid experience and reasoning for why microbiologists don’t propose ‘directed’ mechanisms for many of the chromosomal mutations conferring streptomycin resistance. It’s not a guess and it’s not based on ignorance. This is based on experimental data.
We already know that the ability to metabolize citrate in aerobic conditions was not built into the E. coli. It took a mutation for them to acquire that ability, and Lenski was able to show which mutation that was.[quote=“NonlinOrg, post:206, topic:35830”]
I hereby volunteer my kitchen, although you do understand my/your kitchen are also controlled environments just like Lenski’s lab. The ultimate test is release in nature which has been inadvertently done with many organisms including ab-resistant bacteria.
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First, I doubt you have the needed equipment. At a minimum you need a 37C incubator and an autoclave. You will also need some centrifuges, fume hoods, basic pipettes, and a whole host of other equipment to process DNA.
Second, what are you hoping to prove by moving the bacteria out of the environment they adapted to? Would you try to disprove that polar bears evolved for polar climates by putting them in the Sahara desert?
You are the one claiming that it is a built in mechanism. Therefore, the burden of proof lies with you to demonstrate that it is built in.
What evidence do you have that the E. coli in question have a built in mechanism for putting new promoters in front of the citrate gene?[quote=“NonlinOrg, post:211, topic:35830”]
This is just a story (or a “just so” story) without proof.
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Let’s put it another way. Bacteria and fungi have been trying to kill other bacteria with antibiotics for millions of years. The first generation of antibiotics were discovered in the wild, such as penicillin.[quote=“NonlinOrg, post:211, topic:35830”]
Gotta do better than circular reasoning. You can’t presuppose “evolution” to prove “evolution”.
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Evolution isn’t presupposed. Lenski observed it happening.
See: Awadalla, P. The evolutionary genomics of pathogen recombination. Nat.Genet., 2003, 4, 50-59.
I don’t believe anyone has argued that recombination does not occur in prokaryotic cells. It clearly does. However, genomic recombination in prokaryotes is a general, largely-random process. The discussion of antibiotic resistance in bacteria arose as a comparison to the highly-specific DNA remodeling in developing B and T cells of the immune system. These are very different processes. While there is definitely a built-in process in the B and T cell maturation (V(D)J recombination - Wikipedia), antibiotic resistance happens much more randomly.
Reminder to those who think Natural Selection hasn’t been proved time and time again … below is a description of a simple laboratory demonstration of natural selection … either strongly promoting smaller fish vs. strongly promoting larger fish vs. not strongly promoting either size fish:
3 aquariums were set up, with the same number of randomly sized fish that were successful in reproduction in an aquarium environment.
At regular intervals, a sample of fish were removed from each tank. Tank “A” would have removed the first “x” number of fish that were above a certain size threshold. Tank “B” would have removed the first “x” number of fish that were below a size threshold. And Tank “C” would have removed any sized fish until “x” were removed.
After a significant time period, so that several generations of fish could be born and raised, it was shown that the tank where only the biggest fish were removed (which was to emulate some state laws that prohibited keeping fish that were too small - - thus leaving more small adults to reproduce the next generation) - - the average size of the fish, after several generations of this “selection”, was smaller than the tank where any size fish was removed. And dramatically smaller than the tank where only the smallest fish were removed.
http://www.nycflyfishing.com/The%20Evolutionary%20Effects%20of%20Size%20Limits.htm
I made this graphic to help “Natural Selection Deniers” remember these really important points, which have been discussed to death and are clearly not relevant to any criticisms of Natural Selection::
A) If you have been orbiting a sun for 5 billion years, Entropy does not constrain the process of Evolution in a negative way;
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B) Several aquarium experiments have proved natural selection… there’s nothing to say about it.
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[ Be sure to click on the image to see how really small the surfer is; yes, I knew the image was photo-shopped when I found it. But I think it makes the necessary impression! ]
Who said that? Not me. But this drift has limitations. We have never seen an organism drifting into a completely different one - i.e. “evolution” - Lenski’s E.coli remain E.coli.
Here is my proposal - http://nonlin.org/evotest/ :
How could we actually test Evolution? Lab observation of genetic changes over a number of generations is the ideal experiment, and this has been done many times, but not as a pass-fail test of the Evolution hypothesis. To confirm Evolution and separate it from mere adaptation or genetic drift, a Baseline and a Minimum Threshold have to be established before the actual experiment is conducted. The ideal organism to be tested is very small and is rapidly reproducing. The Baseline would be a fully documented single organism from which all subsequent generations descend while the Threshold for success would be a descendent that under no circumstance would be classified same as the Baseline organism. This may be contentious as biological classifications such as Population, Strain, Species, Genus, etc. are all subjective.
No. Until proven otherwise, it’s just built in flexibility. You keep going in circles.
Why would you think “either/or”?
Kind of like a severe infection that kills 99% of the population? And then it’s passed on like a number of genetic conditions?
Not wiped out but reduced as percent of the population to pre-AB-resistance levels (some were resistant from the beginning, or else all would have died and never developed resistance). AB-resistance is held as “proof of evolution”, but unconvincing.
You misunderstand. Read again.
But that’s exactly the evolution story - gnomes hiding your keys. Why would you believe that without proof? In fact, feel free to believe it, just be aware of your belief without proof.
Mutations happen all the time and are built in biologic mechanisms. Also not proof of “evolution”
I made this comment with regard to your previous statement about mutations conferring antibiotic resistance being ‘devolution’. You wrote: “Antibiotic resistance is not “evolution” but a “devolution” also.” If you assume that was ‘devolution’ then you would conversely assume there must be an earlier, more ‘optimal’ and less ‘devolved’ state. That’s not the case. I’m sorry if that wasn’t clear.
I KNEW IT! … the little buggers. I’m setting the traps tonight …
Sorry but I’m not following your thought process here. You asked about changes like the acquisition of antibiotic resistance in bacteria being derived from a ‘built-in’ mechanism. You asked if one could demonstrate they weren’t from a built-in mechanism. As most know, it’s very hard to prove a universal negative. However, I subsequently explained some of the positive arguments why biologists tend to not invoke the hypothesis of a ‘built-in mechanism’ being behind particular events.
For sure, I’m having trouble getting a clear picture of what the term, ‘built-in mechanism’ means to you. To me, it means a function pre-specified for particular task. Thus mating type switching in yeasts and immunoglobin development in mammals (mentioned earlier in this discussion) would involve specific mechanisms that ensure very specific outcomes. This is in contrast to a case like point mutations arising with random frequency in a ribosomal subunit that happens to allows cells to grow in the presence of streptomycin or even secondary mutations that enable the first mutations to persist in the population when the antibiotic isn’t present. The emergence of these latter mutations do not appear to be ‘actively directed’ by the cells.
“Let your conversation be always full of grace, seasoned with salt, so that you may know how to answer everyone.” -Colossians 4:6
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