Evolution In Action

Jerry Coyne writes in Why Evolution is True, “Microbes like bacteria…can divide as often as once every twenty minutes, allowing us to observe evolutionary change over thousands of generations in real time. And this is genuine evolutionary change, demonstrating all three requirements of evolution via selection: variation, heritability, and the differential survival and reproduction of variants.” (1)

Examples

Richard Lenski of Michigan State University, starting in 1988: (1)(2)

  • Conditions and results:
    • 12 culture lines of genetically-identical strains of E. coli were studied for 18 years (40,000 bacterial generations).
    • The food supply (glucose) was depleted each day (although citrate was added) and renewed the next. This was a test of the microbe’s ability to adapt to a feast and famine environment. Either they had to adapt to eat the citrate or die off.
    • By the 31,500th generation (of 44,000), one of the 12 culture lines developed the capacity to metabolize citrate as an energy source.
    • “Lenski’s experiment is also yet another poke in the eye for anti-evolutionists, notes Jerry Coyne, an evolutionary biologist at the University of Chicago. ‘The thing I like most is it says you can get these complex traits evolving by a combination of unlikely events,’ he says. ‘That’s just what creationists say can’t happen.’” (Holmes, Bob, Bacteria make major evolutionary shift in the lab, New Scientist, 09 June 2008)
    • They surmised that a mutation around the 20,000th generation led to this change.
  • A response:
    • Michael Behe calls this “The Edge of Evolution.” It’s possible for one or maybe two mutations to occur that have an adaptive benefit. This is especially plausible in bacteria because they (1) reproduce quickly, (2) have huge populations and (3) can sustain higher mutation rates.
    • It’s also misleading to imply that the E. coli developed the ability to metabolize citrate, or (TCA):
      • coli has a TCA cycle that allows the bacteria to utilize citrate in its normal oxidative metabolism of glucose.
      • While the tests were done in aerobic conditions, E. coli is normally capable of utilizing citrate as an energy source in anaerobic conditions. It even has an entire set of genes (operon) for citrate fermentation.
        • “A likely scenario is that mutations jammed the regulation of this operon so that the bacteria produce citrate transporter regardless of the oxidative state of the bacterium’s environment.” –Don Batten (2)
        • It’s also possible that another gene which normally transports tartrate, mutated and lost specificity (information) which then allowed it to transport citrate into the cell. A loss of information.
        • “Mutations are good at destroying things, not creating them. Sometimes destroying things can be helpful (adaptive), but that does not account for the creation of the staggering amount of information in the DNA of all living things.” –Don Batten (2)

Barry Hall of the University of Rochester: (1)

  • Conditions and results:
    • A gene from E. coli was deleted. This gene produces an enzyme that allows the bacteria to break down lactose (a source of food).
    • The genes were then placed in an environment where the only food was lactose.
    • Before too long, another enzyme hijacked the function of the missing gene. This enzyme had been mutated which allowed it to break down lactose.
    • A second mutation occurred, increasing the production of this enzyme.
    • A third mutation in a different gene occurred which allowed the bacteria to take up lactose more easily.
    • “Beyond demonstrating evolution, this experiment has two important lessons. First, natural selection can promote the evolution of complex, interconnected biochemical systems in which all the parts are codependent, despite the claims of creationists that this is impossible. Second, as we’ve seen repeatedly, selection does not create new traits out of thin air: it produces ‘new’ adaptations by modifying preexisting features.” –Jerry Coyne, Why Evolution is True (1)
  • Response:
    • “Further analysis of Hall’s research of the coli ebg operon supports, to the idea that bacteria can adaptively mutate under numerous environmental conditions, but with a corresponding reduction in some aspect of the biochemical machinery.” –Tom Hennigan (4)
    • See red section below for more information.

Bacteria’s resistance to penicillin (and all antibiotic resistance):

  • “In 1941, the drug [penicillin] could wipe out every strain of staph in the world. Now, seventy years later, more than 95% of staph strains are resistant to penicillin.” –Coyne
  • “What happened was that mutations occurred in individual bacteria that gave them the ability to destroy the drug.” –Coyne
  • Drug companies came out with a new antiobiotic called methicillin, but even its effectiveness has been reduced as a result of newer mutations.
  • A response:
    • “Non-resistant bacteria commonly become resistant by several different means, most of which have nothing to do with mutations. Palumbi notes that in ‘most cases’ antibiotic resistance results from selection of an existing genetic trait…” –Jerry Bergman (3)
    • Bacteria can obtain a new gene by means of conjugation (where a copy of a plasmid from one bacterial cell is transferred to another bacterial cell), transduction (a virus-mediated transfer of host DNA from one host to another), or transformation (where the bacteria takes up exogenous DNA from its environment). None of these means necessarily involve mutations.
    • “When a bacterial strain has gained resistance to an antibiotic, it is more correct to say that the bacteria has lost sensitivity to the antibiotic.” –Jerry Bergman (3)
    • Bacteria have had resistance to antibiotics long before humans introduced them:
      • “Scientists at the University of Alberta have revived bacteria from members of the historic Franklin expedition who mysteriously perished in the Arctic nearly 150 years ago. Not only are the six strains of bacteria almost certainly the oldest ever revived, says medical microbiologist Dr. Kinga Kowalewska-Grochowska, three of them also happen to be resistant to antibodies. In this case, the antibiotics clindamycin and cefoxitin, both of which developed more than a century after the men died, were among those used.” –Ed Struzik, Ancient bacteria revived, Sunday Herald, Sept. 16, A1
    • In regards to penicillin, microorganisms may produce more of the enzyme beta-lactamase which attacks penicillin. “In 1982, over 90% of all clinical staphylococcus infections were penicillin-resistant, compared to close to 0% in 1952. The reason for the increase was due largely to the rapid spread…of the B-lactamase plasmid.” –Jerry Bergman (3)
    • Bacteria can become resistant by acquiring what are called “multi-drug resistant pumps” from genes that are located on neighboring plasmids (conjugation). These pumps remove many kinds of toxins (like those in antibiotics). The pump mechanism attaches a protein label to the drug and removes it by exocytosis.
    • Bacteria can also become resistant due to mutation, but all the mutations observed so far have resulted in a loss of information.
      • An example is streptomycin, which attaches to a receptor site in the bacteria’s ribosome. A point mutation at the ribosome can prevent the streptomycin from binding to the ribosome.
      • While these mutations help the organism to resist the antibiotic or drug, they often weaken the organism in other ways.
      • “Numerous empirical studies have found that mutations that confer resistant decrease the fitness of bacteria in environments without antibiotics.” –Jerry Bergman (3)
    • Jonathan Sarfati says, “There is not so much an arms race as trench warfare or a scorched earth policy. Many of the changes aredestroying machinery that the enemy could otherwise use. E.g. defenders will destroy their own bridges to prevent an enemy crossing, sabotage their own factories if the enemy is using them to churn out armaments, burn their own crops so the enemy will run out of food.” (5)

Insect resistance to DDT:

  • DDT binds to a specific matching site on the membrane of the insects’ nerve cells, interfering with the functions of the nerve cells. Eventually, the nervous system is no longer able to function and the insect dies.
  • Any mutation that adversely affects the binding site on the nerve cell has the potential of conferring DDT resistance.
  • But extensive studies have shown that these mutations make the insects less fit in the wild. Mosquitos have been specifically researched – they were able to resist the insecticide but had a more sluggish nervous system.
  • “…resistance to poisons is rarely a “free ride” for either insects or other organisms, because the selective trade-offs imposed by pleiotropy often maintain polymorphism either within or between populations of a species. Some populations of Norway rats, for example, have evolved resistance to the rat poison warfarin. Where the poison is in widespread use, homozygotes for the allele that confers resistance are common. But that allele also lowers rats’ ability to synthesize vitamin K, a compound essential in allowing blood to clot, and they bleed more easily. For that reason, in places where warfarin is not used, individuals homozygous for this allele are at as much as a 54 percent selective disadvantage compared to “wild-type” rats, and the allele is far less common. The same sort of phenomenon has been demonstrated for the alleles that confer resistance to DDT and to dieldrin in mosquitoes.” (Levine, J. and Miller, K., Biology: Discovering Life, pg. 257, 1994)

Examples given by Coyne in Why Evolution is True of “evolution” that is nothing more than microevolution via natural selection: (1)

  • The medium ground finch of the Galapagos Islands, whose body and beak size increased during drought conditions so that it could consume larger and harder seeds.
  • The soapberry bug of the New World whose beaks increased in size when it began colonizing newly introduced plants in south Florida and the south-central U.S.
  • The flowering time of the mustard plant (in southern California) came earlier following a five-year drought.

A Great Summary by Jerry Bergman

“Evolution requires information-building mechanisms that add new information to DNA. In virtually all cases, bacteria or insect resistance is a result of the exploitation of existing systems, or is due to a transfer of genes. In the rare cases where a mutation is involved, development of resistance involves only a loss mutation such as one that produces a deformed ribosome. This is confirmed by the fact that resistance is acquired very rapidly, in far too brief a period for the evolutionary emergence of complex biochemical or physiological systems. Mutation caused resistance results in less viability in the wild, and as a result the resistant stains cannot compete.” (3)

Other quotes:

  • “True, breeders haven’t turned a cat into a dog, and laboratory studies haven’t turned a bacterium into an amoeba…But it is foolish to think that these are serious objections to natural selection. Big transformations take time – huge spans of it.” –Jerry Coyne

SOURCES:

(1) Jerry Coyne, Why Evolution is True

(2) http://creation.com/bacteria-evolving-in-the-lab-lenski-citrate-digesting-e-coli#txtRef1

(3) http://creation.com/does-the-acquisition-of-antibiotic-and-pesticide-resistance-provide-evidence-for-evolution

(4) http://creation.com/biblical-ecology#txtRef33

(5) http://creation.com/refutation-of-new-scientists-evolution-24-myths-and-misconceptions-natural-selection

Advertisements

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s