Do you realize ALL evolution works by modifying existing genomes (which Behe disingenuously calls “breaking things”)? Even your Creationist paper admits the changes occurred by “jettisoning non-essential genes” to provide material for fitness gain. So how did the LTEE suffer from GE when in produced an INCREASE in fitness?
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Pretend you are a virus for a moment. You want to stay alive and reproduce as much as possible.
Do you think your “goals” of staying alive and reproducing are met by:
a) Killing your food source (starving) before you can reproduce and survive
or
b) Not killing your food source (not starving) before you can reproduce and survive
Which option seems like the greater fitness improvement to you?
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Remember the niche, Duke!
It might be good to remind people what ‘fitness’ means – it means the organism’s characteristics are a good fit to its environment and lifestyle. That’s the original meaning of ‘fit’, one that has been somewhat obscured by the later meaning of physically fit, e.g. I go to the gym a lot, therefore I’m fit.
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“Other organisms”? Such as…?
Using that as an argument for GE is the equivalent of arguing “People die when you shoot them in the head. Therefore there can’t be any people, because they all get shot in the head.”
Your argument is literally that stupid.
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Indeed, fitness is relative to the niche. I have trouble with absolute fitness. What is it?
Sanford does. That’s what he writes in this article.
As we will see, there has consistently been a net loss of function, a net loss of information, and the E. coli bacteria clearly remain E. coli bacteria – a new form life has certainly not emerged. At best, the genetic changes that have been observed reflect fine-tuning of a few pre-existing genes (microevolution). More fundamentally, in the bigger picture there has been genetic degeneration, which is the consequence of increasing genetic entropy.
And later:
- Will the “evolving” populations eventually display gradual fitness decline and eventual extinction? The LTEE populations have been shown to have substantially faster growth compared to the starting strain, but this is because of just a handful of significantly beneficial reductive mutations (loss-of-function mutations). But even while these few “beneficial” mutations have been happening, a much larger number of mutations have been accumulating which are not beneficial at all. Most of these non-beneficial mutations should be slightly deleterious. 6 out of 12 of the populations have developed defective DNA repair systems and so now are accumulating such slightly deleterious mutations at a much higher rate than normal (Figure 4).
26 Such populations have by now accumulated well over a thousand such slightly harmful (deleterious) mutations per cell. Lenski et al.47 acknowledge that this is resulting in growing “genetic load”.32 The accumulation of these mutations is continuous and clock-like (except when mutation rate changes), and reflects the rusting-out of the bacterial genomes. Even in those populations that have not yet started to hypermutate, the bad mutations are still accumulating much faster than the good mutations. This fundamental problem has been described as genetic entropy (see the book Genetic Entropy available at GeneticEntropy.org or Amazon.com). What can stop this type of reverse evolution? It may take decades or even centuries, but this relentless increase in the population’s genetic load should eventually cause all 12 populations to experience fitness decline – and eventual extinction. This is the essence of genetic entropy.
And more:
Although it will take a very long time, we predict that the LTEE populations will eventually display fitness decline and eventual extinction. This is consistent with our many previous studies involving the general problem of genetic entropy and the associated genetic degeneration of populations (see book Genetic Entropy and related peer-reviewed papers at GeneticEntropy.org) In particular, we have shown that the H1N1 human influenza virus (another classic “model evolutionary population”) has been undergoing genetic degeneration ever since it emerged within the human population about 100 years ago. The human version of H1N1 went extinct in 2009.8
In summation, the most famous evolution experiment ever conducted (LTEE) that is being proclaimed to the world as a dramatic proof of “observable evolution”, is ironically one of the
most powerful demonstrations of genetic entropy and de-evolution.
Perhaps Sanford can make up his mind and talk to Carter?
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By claiming GE is about fitness and referencing Kimura and neutral theory, then discarding the concept of fitness, then inventing some other concept that has to do with total number of functions or “integrity of information in the genome” you can’t quantify, still labeling it fitness, and then by accusing evolutionary biologists of having a specious definition of fitness.
That’s how.
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Absolute fitness is relative to the niche (more properly, to the environment or selective regime) too. It just isn’t relative to other alleles or members of the population. It’s the number of offspring expected to be recruited into the population.
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Ah OK. I was thinking absolute in the sense of not relative to anything as in absolute authority or absolute truth.
oh garsh! 
For one thing, you are pretty easy to be nice to. The other thing is you represent a vastly underrepresented group in these discussions (female YEC). I don’t want anybody scaring you off! (as unlikely as that seems) 
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Regarding your first paragraph, I see him as saying that mutagenesis would work in both the host and in the epidemic. So it seems he’s not making that distinction how you would make it, but I’ve still read about the distinction in the process in his papers.
Regarding your second paragraph, huh? How does preserving the virus without any mutations help, and does it matter if that’s not possible?
Either way the paper you shared seemed to confirm GE except that sometimes a particular mutant gained an a new function and that particular one required a different approach. In general it was interesting, thanks.
I don’t have a problem with saying fitness can increase while GE happens in bacteria. That seems obvious to me. But I’m not the scientist here so IDK. 
Obviously b. I’ve got this part, thanks. 
Already discussed in other threads.
Yep, they need to tune this up and be more clear regarding bacteria. Especially since I read Carter defining certain mutations as increasing information.
To be more clear perhaps, this is what I see:
GE is the concept that natural selection cannot sustainably maintain or increase fitness for any organism over time. Even on rare occasions when function and information may be able to be gained in the short term by a mutant, logically function or information will never be sustained long term because mutation continues, VSDM are inevitable and will decrease fitness. Natural selection’s power varies depending on complexity, population size, and generation time.
(Not sure I like this summary yet either). Terms in biology. Yuck; they’re annoying.
The host population would adapt, and immunization would be nearly entirely effective, thus facilitating the ever desirable herd immunity. Please understand, it is mutation which enables the influenza virus, particularly with respect to the outer coat proteins. This point just doesn’t seem to be registering.
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When biologists come across these ideas they start picturing what they would expect to see in the genetic evidence if GE is accurate.
The very first place to go to is comparative genomics and see what the DNA sequence differences are between vertebrate species. If large swaths of vertebrate genomes can’t be changed much without losing function then we shouldn’t see a whole lot of differences in these regions. However, if large swaths of these genomes can be randomly change without any real impact then we should see very little conservation in much of these genomes and conservation in just the relatively small fraction of functional regions.
What do we see? As I spoke about in another post, when we compare the human and mouse genome we see 85% similarity in known functional coding regions. In non-functional regions, such as the vast majority of intron sequence, the similarity is barely distinguishable from random sequence. Vast swaths of the genomes have been changed, and both species survive just fine.
This is just one reason out of many why GE doesn’t pass the smell test.
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Okay. So if a virus naturally attenuating in virulence due to the accumulation of mutations increases the likelihood of survival and reproduction for the virus, at what point would this virus go extinct by increasing it’s ability to survive and reproduce?
Again, pretending you are the virus and you want to live/reproduce–you’ve choosen option b) Not killing your food source (i.e. natural attentuation)–why would this process cause you to die?
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Full disclosure: I am a geoscientist, not a biologist.
Perhaps there is a relatively simple test for the GE “hypothesis”. Schuenemann, V., Peltzer, A., Welte, B. et al. (2017) report the sequencing of over 90 individual Egyptian mummies, from the New Kingdom (~16 th century BC) to the Roman period.
Given the now-vast libraries of modern genomes, it should be relatively simple to point the differences between the less-degraded Egyptian DNA and the doomed modern population.
(If of course there is an objective metric to measure GE in physical samples).
For even more testing, see if anyone can blindly diferentiate an ancient genetic sample from a modern one.
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A lot of assumptions about evolution there.
It doesn’t increase its ability, it’s merely maintaining it in the short term.
They aren’t assumptions. One of the things creationists do a lot is call evidence “assumptions” when they don’t like it.
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Why would the careful husbandry of your food source be a short-term project? Wouldn’t your virion “children” have the set of instructions for how to treat their food source?
Children don’t always take advice from their parents. Maybe the instructions get jumbled up at some point for one of your virion “kids” and they accidentally kill their host and starve. Oops.
But, the rest of your virus children followed the instructions and get to stay alive. Why would these instructions for how to stay alive only be temporary?
Perhaps more importantly, do you think we should interpret the ability to stay alive and reproduce as “trending toward death?”
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