No. How?
Simple genetic change does not extrapolate automatically to bacteria-to-human “evolution”.
It’s not clear what you argue. It seems you agree immunity is a built in mechanism and you don’t know Lenski’s E-coli don’t have a similar built in mechanism.
This is just a story (or a “just so” story) without proof.
Gotta do better than circular reasoning. You can’t presuppose “evolution” to prove “evolution”.
Correction: “my personal immune system is built-in” Period. There is absolutely no need for “as a result of evolution”. You’re trying to establish that hypothesis, remember? It relates because E.coli also have built in adaptation mechanisms - one of them observed by Lenski.
Antibiotic resistance is a temporary and reversible phenomenon currently present only in extreme, hospital-like environments (as you note), hence not “evolution”.
Well, if they don’t take over, then no “evolution”, right? Where is the Neanderthal and all others? Chimps are around but supposedly they’re “cousins”, not ancestors. And how do you know “advantage”? That’s unknowable except through survival. Is “advantage” aka “fitness” even a thing? Sewage treatment plants are controlled environments themselves so, sure, under controlled conditions a Chihuahua is an “evolved” wolf.
Evolution has more dead ends than successes. It is sort of like starting a restaurant . Some do great, many fail. Some who do great for a while then fade and close. Some develop into chains, spin off other eateries. Some find a niche and thrive in a local area but cannot make it elsewhere. I agree that success is only knowable through survival, but most are not successful.
I’m afraid this isn’t the same at all. Every single human goes through the DNA shuffling for B and T cell lineages. The same is not true for E. coli and the development of the aerobic utilization of citrate.
I used the example of NFL player Daniel Fells, who likely picked up the infection in an NFL locker room. I’ll send another URL because the one I used with Fells may not have been the best example. https://www.bostonglobe.com/sports/2013/10/26/buccaneers-dealing-with-mrsa-outbreak/2JxLajA7nNdZXec8kKq4kI/story.html There we go, definitely NOT in a hospital-like environment. It would be great if you were correct about how antibiotic infection doesn’t spread, but it just isn’t true. My daughter picked one up “out of the blue” last November. Luckily, we got her to an ER before it had a chance to spread much. I have no idea where she picked it up, but it wasn’t a “hospital-like environment”, either.
I volunteer my kitchen. Most strains of E. coli are not pathogenic, and that includes the B strain used in the Lenski experiment. You’ve already got loads of E. coli in your gut, after all.
So there’s no need for silly little lab rules like “no eating or drinking in the lab” and “wash your hands thoroughly before leaving the lab”?
I’m ok with classifying lab strains as “generally nonpathogenic”, but we take precautions to avoid the possibility of rare, but potential pathogenic events. We do indeed have loads of E. coli (and other bacteria!) in our guts. These too, are pathogenic under unusual circumstances – like a perforated colon.
Sure, there are reasons for the rules, including avoidance of chemical hazards and preventing exposure of immune-compromised people to normally nonpathogenic agents. The rules are pretty minimal though – we can carry food through our BL1 lab provided it’s covered with a paper plate, for example.
I don’t know about you, but we have raw chicken in our kitchen at home pretty frequently, and that’s a lot more likely to generate a pathogenic event than these bacteria. Most store-bought chickens are contaminated with either Campylobacter or Salmonella, both BL2 pathogens. I’m not saying I intend to start culturing strain B E. coli in my kitchen, but if I did, I’d rank it well down the list of hazards in my home.
Agreed, I just brought up the hypothetical situation to illustrate for @NonlinOrg that a small portion of Lenski’s organisms, although adapted to lab growth, could grow and adapt (and evolve) outside the lab. It was not a comment on relative safety issues.
Me: Are you not aware that lab strains of E. coli have been deliberately crippled?[quote=“NonlinOrg, post:211, topic:35830”]
No. How?
[/quote]
They carry many mutant alleles that prevent recombination, making them better hosts for cloning DNA using plasmids. Since recombination is a major source of genetic variance (that is ignored by laypeople in favor of mutation), that makes Lenski’s results a gross underestimate of the capabilities of evolution in nature!
How can you hold yourself up as understanding biology better than biologists do, when you lack even a Wikipedia-level understanding? Isn’t that a tad arrogant?
For E. coli, this is not a concern for the lab strains, but it is for contaminants in their cultures. For a host of other things in the lab, there’s definitely a need for those rules.
I’ll drink a liter of E.coli K12 if you’ll drink a milliliter of phenol, OK? 
Supposedly? No, definitely; there’s zero evidence that chimps are ancestors, and that’s from a massive amount of DNA evidence.
Perhaps you should consider a basic biology course before posturing as though you know it all.
Hahahaha, I’m still going to pass on both, but point taken!
False. There’s a reason why the major arm of your immune system is called “adaptive.” Check it out.
This is fact, not hypothesis. Your acquired immune system functions as a result of selection of NEW genetic variants that are subject to strong selection. It only takes 2 weeks for you to generate new, incredibly specific and avid, protein binding sites, precisely what Behe claims is beyond the edge of evolution.
If you’re deficient in the recombination mechanism for generating NEW genetic variants, you’ve only got the built-in part, which means you don’t have much of an immune system. Just a couple of many examples:
Immune response:
It’s nothing at all like the adaptive immune response. I provided links to a few papers in my last response.
Mix with wild-type where?:
In the outside environment. These strains that persisted with resistance were isolated outside the lab.
Antibiotic resistance goes away eventually.:
Consider what mechanisms would favor that and whether other mechanisms would compensate. This is discussed in the articles I cited.
I sense there is an idea that any particular bacterial species has an ideal genotype or that there is a canonical set of conditions in the wild that all the bacteria within a particular species are adapted too. That’s not the case. In ‘the wild’ and even ‘in the lab’, bacteria experience many different environments. There is no genome that works ‘best’ in all experienced conditions. Instead, there is dynamic, shifting change in the genomes that goes on all the time.
In microbiology, we’ve know that for decades. Over time, we always see drift in our isolated strains. The longer the strains are propagated or the more generations they go through, the greater the difference form the original bacterium isolated. This isn’t devolution’: This is simple drift. That’s why, for example, that microbiologists freeze or lyophilize strain cultures early after initial collection (if possible). That is so they can go back the the earliest generations as a reference. With the advent of lower cost genomic screening, we can see the same in genetic surveys of bacterial isolates in the wild. There is diversity and constant diversification.
One goal (of many) for Lenski’s long term culture experiment was to quantitate and understand how lineages of bacteria change over time. And he chose to examine this under a simple set of conditions. The growth media, time between splittings and growth temperatures were kept constant. This was almost a constant environment. Well, in all senses but one: The bacteria themselves. They were allowed to propagate within the environment; which meant genetic drift. With every successive splitting of the cultures, each bacterium faced a slightly different set of siblings and a different distribution and set of genes in the population. Bacteria competed with their siblings. And Lenski’s group observed the shifting populations and the genetic lineages over time. Because they’d taken samples at each generation they could also ‘play back’ situations and identify the key mutations behind the evolutionary sweeps. The main message from this work: Even in what would appear to be a ‘static’ external environment, there is always selection and genetic drift. We also can see that there is no singular ‘canonical’ genome that’s optimal for any single, external environment, to say nothing of what happens in the many niches organisms experience ‘in the wild’
First, sorry it has taken me a few days to reply! Time has been in short supply.
Next, yes, absolutely I am saying the tree of life is more than a product of Darwin’s imagination. It was based on Linnaeus’s classification scheme that many people first began to look and suspect that life must evolve in some way: Darwin merely did the legwork and meticulous documentation to make the idea hold up, and provided the correct mechanism of natural selection to explain it.
You could call it a pattern of nested hierarchies if you like it better. Nested hierarchy means that life falls into a pattern such that all dogs form one group, which falls into a larger group of wolves, which in turn falls into a larger group of canids including the coyote and jackal. This much at least creationists will agree with, I believe: dogs, wolves, coyotes, and jackals can interbreed and therefore are uncontroversially the same ‘kind,’ descended from a common ancestor.
Although there are some few historical reports of foxes breeding with dogs, they are not considered reliable. No one to date has found genetic evidence of canine/vulpine interbreeding. Yet some creationists will say that all canids are the same kind, including foxes, wolves, raccoon-dogs, etc.
But it doesn’t stop there. Look further for ‘related’ species and we find ourselves in the order Carnivora, with cats, dogs, bears, weasels and seals. All these creatures are more like each other in many ways than they are like rats or bats or monkeys or us. Here is a great article describing why the similarities should not be ignored:
And of course, as expected by the theory of common descent, we don’t stop there. Because all members of Carnivora are also members of Mammalia, along with many other species, all of which fall into their own orders and classes and genuses of hierarchically nested species. And mammals are grouped with the other tetrapods, and all of those are vertebrates, and all vertebrates are in the animal kingdom, and all animals are eukaryotes.
That’s not the imagination of Darwin speaking. That’s science. And here’s the kicker: when we started looking at the DNA of all these animals in all these species and genuses and families and classes and orders and phylums and kingdoms, we found that with a few minor adjustments, the evidence overwhelmingly confirmed the ‘tree of life’ pattern of nested hierarchies that we had placed all these animals in. A raccoon dog doesn’t have DNA halfway between a raccoon and a dog, it has DNA closely related to the group of South American canids that it is evolutionarily supposed to have come from. And that DNA is more similar to a cat’s than either would be to any non-Carnivora mammal. And you can keep going all the way back up the tree of life, and these predictions will hold true.
Nor can the similarities be explained simply by morphological similarity. An elephant is most closely related to dungongs, manatees, and hyraxes. Hyraxes you may be familiar with as the ‘rabbit that chews its cud’ referenced in the Bible—they’re not really rabbits at all, of course, but the King James translators went with what their audience would recognize.
But who would predict that these very different creatures would have similar DNA? Only an evolutionist.
Unless, as you say, creationism would make the same predictions. In which case, I would dearly love to see the details!
You do understand that you adding “bacteria-to-human” evolution is a rather blatant attempt to create a strawman argument. Who said anything about Evolution from “bacteria to humans”?
Are you some kind of God? … who knows what the end point of the evolutionary change will be?
ANY change in the genetics of a population Is Evolution. Who can say what the end point will be, or could be.
You can’t be serious with any of this, can you? These are the worst category of refutations.
If we don’t know what all the genes do, how can you expect even laboratory-induced mutation to lead to dramatically different life forms.
And your continued fixation on dramatic changes in behavior or appearance can only be based on one premise: that speciation is even possible.
So are you prepared to accept Speciation as real? If not, there’s no point in discussing how to obtain dramatic changes from speciation!
Not only that, but speciation doesn’t necessarily depend on changes in behavior or appearance.
“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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