Expelled: No Intelligence Allowed

Sounds good to me. We are still made of inanimate matter you know..

This does not explain where the methicillin resistant gene came from in the first place. It did not exist until recently after methicillin was developed by humans, and we artificially selected for resistant strains. If you look at the gene or genes involved in resistance you will see they are homologous to other genes that always existed in bacteria, only with small mutations.

 

Evolution, shmevolution. God just made those supergerms to punish us for not going to church enough.

 

Basically, the science you're quoting above is incorrect. Through evolution, organisms can regain any temporary loss of functionality while retaining resistance. That's what makes these resistant bacteria such pests.

These ought to be publicbly accessible, but if not, here are the full abstracts:

Int Microbiol. 1998 Dec;1(4):265-70. Links

Bacterial evolution and the cost of antibiotic resistance.

Lenski RE.
Center for Microbial Ecology, Michigan State University 48824, USA. [email protected]
Bacteria clearly benefit from the possession of an antibiotic resistance gene when the corresponding antibiotic is present. But do resistant bacteria suffer a cost of resistance (i.e., a reduction in fitness) when the antibiotic is absent? If so, then one strategy to control the spread of resistance would be to suspend the use of a particular antibiotic until resistant genotypes declined to low frequency. Numerous studies have indeed shown that resistant genotypes are less fit than their sensitive counterparts in the absence of antibiotic, indicating a cost of resistance. But there is an important caveat: these studies have put resistance genes into naive bacteria, which have no evolutionary history of association with the resistance genes. An important question, therefore, is whether bacteria can overcome the cost of resistance by evolving adaptations that counteract the harmful side-effects of resistance genes. In fact, several experiments (in vitro and in vivo) show that the cost of antibiotic resistance can be substantially diminished, even eliminated, by evolutionary changes in bacteria over rather short periods of time. As a consequence, it becomes increasingly difficult to eliminate resistant genotypes simply by suspending the use of antibiotics.

Proc Biol Sci. 1997 Sep 22;264(1386):1287-91.
Related Articles, Links

[SIZE=+1]Adaptation to the fitness costs of antibiotic resistance in Escherichia coli.[/SIZE]

Schrag SJ, Perrot V, Levin BR.

Department of Biology, Emory University, Atlanta, GA 30322, USA.

Policies aimed at alleviating the growing problem of drug-resistant pathogens by restricting antimicrobial usage implicitly assume that resistance reduces the Darwinian fitness of pathogens in the absence of drugs. While fitness costs have been demonstrated for bacteria and viruses resistant to some chemotherapeutic agents, these costs are anticipated to decline during subsequent evolution. This has recently been observed in pathogens as diverse as HIV and Escherichia coli. Here we present evidence that these gentic adaptations to the costs of resistance can virtually preclude resistant lineages from reverting to sensitivity. We show that second site mutations which compensate for the substantial (14 and 18% per generation) fitness costs of streptomycin resistant (rpsL) mutations in E. coli create a genetic background in which streptomycin sensitive, rpsL+ alleles have a 4-30% per generation selective disadvantage relative to adapted, resistant strains. We also present evidence that similar compensatory mutations have been fixed in long-term streptomycin-resistant laboratory strains of E. coli and may account for the persistence of rpsL streptomycin resistance in populations maintained for more than 10,000 generations in the absence of the antibiotic. We discuss the public health implications of these and other experimental results that question whether the more prudent use of antimicrobial chemotherapy will lead to declines in the incidence of drug-resistant pathogenic microbes.

Curr Opin Microbiol. 1999 Oct;2(5):489-93.
Related Articles, Links

[SIZE=+1]The biological cost of antibiotic resistance.[/SIZE]

Andersson DI, Levin BR.

Department of Bacteriology Swedish Institute for Infectious Disease Control S-17182, Solna, Sweden. [email protected].

The frequency and rates of ascent and dissemination of antibiotic resistance in bacterial populations are anticipated to be directly related to the volume of antibiotic use and inversely related to the cost that resistance imposes on the fitness of bacteria. The data available from recent laboratory studies suggest that most, but not all, resistance-determining mutations and accessory elements engender some fitness cost, but those costs are likely to be ameliorated by subsequent evolution.

Genetics. 2000 Mar;154(3):985-97.
Related Articles, Links

[SIZE=+1]Compensatory mutations, antibiotic resistance and the population genetics of adaptive evolution in bacteria.[/SIZE]

Levin BR, Perrot V, Walker N.

Department of Biology, Emory University, Atlanta, Georgia 30322, USA. [email protected]

In the absence of the selecting drugs, chromosomal mutations for resistance to antibiotics and other chemotheraputic agents commonly engender a cost in the fitness of microorganisms. Recent in vivo and in vitro experimental studies of the adaptation to these "costs of resistance" in Escherichia coli, HIV, and Salmonella typhimurium found that evolution in the absence of these drugs commonly results in the ascent of mutations that ameliorate these costs, rather than higher-fitness, drug-sensitive revertants. To ascertain the conditions under which this compensatory evolution, rather than reversion, will occur, we did computer simulations, in vitro experiments, and DNA sequencing studies with low-fitness rpsL (streptomycin-resistant) mutants of E. coli with and without mutations that compensate for the fitness costs of these ribosomal protein mutations. The results of our investigation support the hypothesis that in these experiments, the ascent of intermediate-fitness compensatory mutants, rather than high-fitness revertants, can be attributed to higher rates of compensatory mutations relative to that of reversion and to the numerical bottlenecks associated with serial passage. We argue that these bottlenecks are intrinsic to the population dynamics of parasitic and commensal microbes and discuss the implications of these results to the problem of drug resistance and adaptive evolution in parasitic and commmensal microorganisms in general.

 

I disagree with Alric on this point regarding the definition and prefer a more focused definition of evolution, like from the dictionary:

Biology. change in the gene pool of a population from generation to generation by such processes as mutation, natural selection, and genetic drift.

or

Darwin's definition: descent with modification. The term has been variously used and abused since Darwin to include everything from the origin of man to the origin of life.
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I see the origin of life from inanimate matter as a separate question (the theory of abiogenesis).

 

The same amount information is present in two genes if they are of equal length. Amount of information is independent of its activity or lack thereof. That information business is an erroneous ID misconstruction. All that matter is which genes are fittest to their environment.

MegansPrius:

I also like your definitions better. I am just making the point to Wildkow that nothing in that definition is incorrect.

 

My definition of evolve, not from any books or someone Else's words but what I think evolution is.
It is where slight variations occur in a population, the variations which are to the advantage of the organism will be perpetuated in the offspring of the more successful of the varied population while the organisms without the mutation would not thrive therefore would breed less. The organisms which have the mutation may breed with those that don't and some offspring will have the mutation to a more or less degree, the most successful will breed and expand numbers within the population. Slowly over time new species can come into being

 

Go watch macaroni boiling in a pot. Notice the structure of the convection cells. Were they designed?
Here's a hurricane. Look at all that structure. Was it designed?
Here's a rainbow. Look at all that structure. Was it designed?

Which parts of your body are made of animate matter, and which parts are made of inanimate matter?

 

Pat, it's important to note that mutation is only one source of the variations which you (& Darwin) described.

Another important source of the variations is genetic recombination -- which is a guaranteed result of every sexual reproductive event. Still, whether or not the variations resulting in this way are adaptive / advantageous, is left to random chance. Indeed, most of these new variants are cosmetic, with little survival value.

Must, maybe, just maybe, some of the new modifications will be adaptive to changing conditions.

I'll also note that this method of genetic recombination is restricted to sexually reproducing (eukaryotic) organisms. (Yes, Bio is full of exceptions to rules; yes there are some bacteria manifesting "para-sexual" methods such as conjugation).

Now, how did I get roped in to this mess !?

 

You are wrong. This is a straw man raised by by IDsts, specifically Dembski. There is no difference in information content between a gene with a squence that produces a deleterious mutation and another that produces a beneficial one. The only difference between the two is that the deleterious mutation will be selected against.

Also, it would not be a problem if the information content of a gene increases. Other methods of genetic change are gene duplications and insertions that increase gene length. You can increase the amount of information in a system by spending energy. For example I just increased the amount of information in the Priuschat server hard disc by typing this words. The energy comes from he food I ate and ultimately from the Sun.

 

To go further, "information" is not a factor in evolution, whether there is more, less, or the same. Only fitness is. Loss of function mutations, if they lead to an increased chance of survival and reproduction, can be selected for and drive evolution.

In fact, it may be that genetic changes themselves are not necessary for evolution at all -- evolution only requires heritable traits that produce different degrees of fitness. For the vast majority of life (plants, animals), genetic changes in the germ line are the only inheritance we know of. For bacteria, phages and epigenetic changes may also be heritable -- phages in particular blur the lines since they can move between organisms and even species and evolve mostly independently of the host organism. For some animals and humans in particular, teachable behaviours may serve much the same role as genetic changes: they can be selected for or against, and they can be passed on to the next generation. That starts leading us down the road to some of the newer and less tested ideas such as the "meme", so I think for this discussion, it's probably best to leave it there.

 

Tons of references on genes and information.

CB102: Mutations adding information

The point on energy is just the correct interpretation of the 2nd law of thermodynamics. Not the fantastical creationist construct:

CF001.2: Thermodynamics universal

 

You had said:
Quote:
Originally Posted by Wildkow
If testability is the crucible within which ID is either rejected or accepted as science then it should be fair turn around to apply the same standard to Darwinism. Let’s start with the origin of life is that testable? Answer: nope ergo Darwinism is not science. In fact Darwinism comes up against one of the immutable laws of Biology and that is that life only comes from life otherwise known as biogenesis.

And I replied: You're redefining words to win your argument.

In biology, evolution is the process of change in the inherited traits of a population of organisms from one generation to the next.

Origin of Life = abiogenesis


I brought up the definition aspect because you kept including abiogenesis in your "proofs" against evolution (see above). While theories of abiogenesis include concepts derived from evolution, the theory of evolution does not address abiogenesis.

If you don't like evolution being "change over time," or "descent with modification over time," or "the process of change in the inherited traits of a population of organisms from one generation to the next," all widely accepted definitions of evolution which are saying the same thing, perhaps you ought to consider that you might be arguing against a straw man of your own creation rather than an accepted definition of evolution.

Two of the definitions you cite do seem rather outdated:

Robert Chambers: the doctrine according to which higher forms of life have gradually arisen out of lower..
Answers.com: A gradual process in which something changes into a different and usually more complex or better form
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These both impose a judgment on the "quality" of evolution, and while that may have been accepted in the last century, it is no longer the case. For example, a mutation can be briefly favorable and then disastrous later. It was certainly an advantage to the Dodo, lacking predators, to stop wasting resources on the ability to fly. While that adaptation may have proved valuable for many centuries, it proved catastrophic as soon as the Dodo encountered an able predator like man. Hence, "better" in one instance can be disastrous later, and isn't part of the definition.

No, these results are not all "anticipated; some are observed:
Current Opinion in Microbiology
Volume 2, Issue 5, 1 October 1999, Pages 489-493

In the majority of studies performed, resistance caused by target alterations has been found to engender some cost to fitness (Table 1), but mutants with no measurable costs have also been observed. One example of a ‘no cost’ resistance mutation is the 42nd codon AAA (Lys)→AGA (Arg) substitution of the rpsL gene, responsible for resistance to high concentrations of streptomycin in S. typhimurium and other enteric bacteria [7 and 8]. Other substitutions at the same position cause severe reductions in fitness both in vitro and in mice [7 and 12], whereas these rpsL AGA mutations appear to be selectively neutral and may even confer a slight advantage over wild type [7].

Why, in the absence of antibiotics, evolution ameliorating the cost of resistance is more common than reversion to drug sensitivity has been attributed to two processes: compensatory mutations being more common than true reversion (which is commonly restricted to single nucleotide substitution), and the population bottlenecks associated with serial passage [28].

The degree of restoration of fitness by the compensatory mutations varies greatly, and in some cases restoration appears complete, whereas in others it is only partial [7, 8 and 12. S Schrag, V Perrot and BR Levin, Adaptation to the fitness cost of antibiotic resistance in Escherichia coli. Proc R Soc London 264 (1997), pp. 1287–1291. View Record in Scopus | Cited By in Scopus (129)12].

Although it has been long thought that antibiotic-resistance genes and accessory elements would engender a cost in the fitness of bacteria, the actual evidence for this being the case is, at best, modest and that which has been gathered recently does not paint a rosy picture for the future of the resistance problem. Resistance mutations, such as those found in the bacteria from patients treated with antibiotics, have virtually no cost when measured by competition experiments in vitro or in experimental animals. Moreover, in those cases where resistance mutations and accessory elements engender a cost, subsequent evolution in the absence of antibiotics commonly results in the amelioration of those costs rather than reversion to drug sensitivity. If these laboratory observations reflect the situation for bacteria in hospital and community acquired infections, even low levels of antibiotic use could be sufficient for the ascent and long-term persistence of resistance [5 and 6•. DJ Austin, KG Kristinsson and RM Anderson, The relationship between the volume of antimicrobial consumption in human communities and the frequency of resistance. Proc Natl Acad Sci USA 96 (1999), pp. 1152–1156 References [5 and 6] illustrate two different approaches to the development of mathematical models of the population genetics and epidemiology of antibiotic resistance. These two papers are part of a growing literature on this subject by population and evolutionary biologists. These theoretical studies provide the necessarily quantitative information needed to unambiguously identify and evaluate the role of the different factors contributing to the ascent and maintenance of drug resistance, and to interpret the results of epidemiological studies of the relationship between drug use and drug resistance. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (265)6].
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Or
Genetics, Vol. 154, 985-997, March 2000, Copyright © 2000

One effect of the continued use of antibiotics is to make compensatory evolution all that more likely than reversion. There is no evolutionary alternative for bacteria in hosts that are under treatment or in an environment that abounds with active antibiotics. In the presence of these chemotherapeutic agents, sensitive revertants would be at a selective disadvantage, even if they may be more fit than resistant bacteria in the absence of these drugs. Stating this another way, as a consequence of the extensive use of antibiotics during the past half century, we have established not only an environment where not-so-natural selection favors resistance, but also an environment where selection would almost neccesarily favor mutations that compensate for the fitness costs of those resistance genes and plasmids, rather than drug-sensitive revertants and segregants. Moreover, it may well be that this compensatory evolution in bacteria has established genetic backgrounds where susceptible revertants (or segregants, in the case of plasmids) are at a selective disadvantage relative to resistant, as has been observed experimentally by B[SIZE=-1]ORMAN[/SIZE] et al. 1996 and S[SIZE=-1]CHRAG[/SIZE] et al. 1997 for chromosomal resistance and by B[SIZE=-1]OUMA[/SIZE] and L[SIZE=-1]ENSKI[/SIZE] 1988 and M[SIZE=-1]ODI[/SIZE] and A[SIZE=-1]DAMS[/SIZE] 1991 for plasmid-borne resistance.
​

To say that bacteria surviving antibiotics have not demonstrated "evolution" but rather "adaptation" seems again like a game of semantics. As noted above, short-term loss of function is often restored by subsequent evolution.

The scientists working on these problems of resistance are in fact using the theory of evolution in their daily work.

Individual organisms don't evolve; populations evolve. I don't know that an increase of information within the gene is necessary; the information may already be present in the gene but in an inactive state. Perhaps someone else can answer this one. EDIT: see Alric's much better answer to this question above.

But "genetic information" does not always seems to correspond to an an organism's complexity. 80-90% of the human genome is classed as "junk DNA" for which the purpose is not known. And amphibians contain far more genetic information than we do, but seem less complex.

Genome Sizes
Even though Psilotum nudum (sometimes called the "whisk fern") is a far simpler plant than Arabidopsis (it has no true leaves, flowers, or fruit), it has 3000 times as much DNA. No one knows why, but 80% or more of it is repetitive DNA containing no genetic information. This is also the case for some amphibians, which contain 30 times as much DNA as humans do but certainly are not 30 times as complex.
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It is your prerogative to be wrong.

Exactly.

 

That's an ironic statement coming from you considering that ID "experts" are essentially trying to change the definition of science into something so silly as to allow astrology to be considered scientific theory.

wildkow, you continue to avoid the discussing the most important organization behind ID: the Discovery Institute. What are you afraid of?

 

No. The theory of evolution is a tool, giving us understanding into how things work.

Darwin himself speculated on the Origin of Life but excluded it from his theory:

In other countries, where Darwin's Origin, published the same year as Pasteur's studies, had an influence, which in France it tended not to, abiogenesis was still regarded as a viable notion. Although Darwin added the phrase "by the Creator" into his final paragraph in the second (1860) edition, and Huxley had also publicly stated that life may have been originally created, this was never understood to be part of the evolutionary mindset, and it was not long before people began to speculate on how life began. Darwin himself did, in a letter to his botanist friend Joseph Hooker in 1871, he wrote:

"It is often said that all the conditions for the first production of a living organism are now present, which could ever have been present. But if (and oh! what a big if!) we could conceive in some warm little pond, with all sorts of ammonia and phosphoric salts, light, heat, electricity, &c., present, that a proteine (sic) compound was chemically formed ready to undergo still more complex changes, at the present day such matter would be instantly absorbed, which would not have been the case before living creatures were found."
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In print, though, he restrained from speculation, noting that "In what manner the mental powers were first developed in the lowest organisms, is as hopeless as how life itself first originated. These are problems for the distant future, if they are ever to be solved by man." (Descent of Man, chapter 2, 1871). In an essay to the Atheneum in 1863, Darwin wrote upon heterogeny "as the old doctrine of spontaneous generation is now called", in which he noted that a "mass of mud with matter decaying and undergoing complex chemical changes is a fine hiding-place for obscurity of ideas". He argued that while it is true that at one time "there must have been a time when inorganic elements alone existed on our planet", "our ignorance is as profound on the origin of life as on the origin of force or matter", and denies that the theory of evolution requires that life continuously arises.

That is why I brought up the definition issue several pages back. While "descent with modification" is good enough for me, something more specific might be:

In biology, evolution is the process of change in the inherited traits of a population of organisms from one generation to the next.
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That covers the most essential points (change, descent, populations, time). If you would like to propose another, please do so.

Well, there is an enormous amount of information on the theory of common descent, if that is what you wish to argue about. You can read some of it here.

I think Alric is better suited to discuss genes and information with you than I. But the number of genes does not necessarily always correspond to complexity. Try reading.
Why Do Humans Have So Few Genes?

But it turns out that we have only about 25,000 genes--about the same number as a tiny flowering plant called Arabidopsis and barely more than the worm Caenorhabditis elegans.

​

I've been trying to link to publicly available sources, but our internet connection is pretty wonky at home (i.e., provided as free unreliable wireless) so I can't always check them in a timely manner.