Question 041117b: Are the antibiotic-resistant strains
of bacteria a proof for evolution?
Answer 041117b: No, they aren't. Evolution is the formation
of new, more complex and better adapted species due to mutation and
selection. Antibiotic resistance is caused mainly by gene transfer,
and not by mutation and the bacteria are better suited for the local
environment. But can this really be called "evolution"? I do not think
so, and here are my reasons.
1. Most antibiotic resistance comes not from mutation,
but from plasmid transfer of a gene from other organisms. This transferred
gene makes a protein that destroys the antibiotic.
Citation: "Most examples of antibiotic resistance in pathogenic
bacteria are not the result of a mutation that alters the protein that
the antibiotics attacks, although this mechanism can occur in laboratory
experiments. Instead, antibiotic resistance in nature usually involves
the production by the bacterium of enzymes that alter the antibiotic,
rendering it inactive. The major factor in the spread of antibiotic resistance
is transmissible plasmids, which carry the genes for drug-inactivating
enzymes from one bacterial species to another. Although the original source
of the gene for these enzymes is not known, mobile genetic elements (transposons)
may have played a role in their appearance and may also allow their transfer
to other bacterial types"
(Reference: Kadner, R.J. (1997): Bacteria and other Monerans.
The New Encyclopaedia Britannica. Vol. 14, 570-585).
2. If mutations occur and antibiotic resistance results, it is
the negative mutation that makes a protein inactive.
Citation:
"Antibiotics usually enter bacterial cells by means of preexisting
carbohydrate-, amino acid-, or ion-specific transport systems, whose
natural substrates they mimic (Brown, 1977). Consequently, mutants deficient
in one of these transport systems are resistant to an antibiotic entering
through this system."
"From cultures of sensitive bacteria, treated with the antibiotic
streptozotocin, two classes of resistant mutants can be isolated: 1)
mutants, resistant under all conditions tested to even the highest doses
of the antibiotic. These are either pleiotropic-defective pts-mutants,
or more frequently, mutants lacking a transport system (enzyme IINag-complex
of PEP-dependent phosphotransferase system) encoded by the gene nagE.
This gene is inducible by N-acetyl-glucosamine and seems to be part of
the nag operon. The transport system in question is responsible for the
uptake of N-acetyl-glucosamine, of D-glucosamine and of streptozotocin;
2) conditional resistant mutants which are unable to energize or
to synthesize the streptozotocin transport system under certain growth
conditions but do have the transport activity under other conditions. These
include a) mutants auxotrophic for amino acids, vitamins, or nucleotides,
b) mutants negative or sensitive to carbohydrates in the medium,
and c) mutants with defects in energy metabolism such as PEP synthesis."
(Reference: Lengeler, J. (1980): Characterization of Mutants of Escherichia
coli K12, Selected by Resistance to Streptozotocin. Molecular and
General Genetics 179, 49-54).
3. The original experiment of antibiotics resistance by Lederberg
showed that the resistance already existed before the antibiotic was
added to the bacteria colonies. So, antibiotics did not cause the mutations/gene
transfers.
(Reference: Lederberg, J. und Lederberg, E. M. (1952): Replica
plating and indirect selection of bacterial mutants. Journal of Bacteriology
63, 399-406)
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