BIO 370 Lecture Notes - Lecture 20: Allele Frequency, Wild Type, Membrane Protein
Antibiotic-resistant strains of bacteria have resistance mutations that modify the chemical
opositio of a atiioti’s target (e.g., a erae protei, a riosoal RNA, a opoet
of the cell wall).
Such modifications are highly beneficial in the presence of antibiotics, but they can have
substantial fitness costs to the bacterial cell in the absence of antibiotics, because they hinder
or eliminate the function of highly adapted elements of the cellular machinery.
Because of the fitness costs, one would imagine that in the absence of antibiotics, resistant
strains would decrease in frequency, and this is sometimes the case.
However, as illustrated in the next slide, resistant strains often remain at high frequencies even
in the absence of antibiotics.
The main reason for this is compensatory mutations.
What is a compensatory mutation?
do not reduce the degree of resistance, but
do reduce or eliminate the fitness costs associated with the resistant phenotype
Given that bacteria are haploid, and using R for resistant and r for sensitive at one locus, and C
for compensated and c for uncompensated at another locus, a bacterial cell can be:
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The resistance allele R replaces the sensitive allele r, and then the compensatory allele C
replaces the wild type c.
In
the absence of antibiotics, the wild type rc is the most fit. The resistant allele R imposes a
significant fitness cost that is largely ameliorated by the compensatory allele C. In the presence
of antibiotics, the wild type has very low fitness. Under these conditions, the resistant allele R
provides a large fitness benefit and the compensatory allele C then provides an additional
fitness advantage.
Polygenic Traits Can Exhibit Nearly Continuous Variation
The recognition that many traits are polygenic was a first step in reconciling Darwinian natural
selection with Mendelian inheritance.
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Document Summary
Antibiotic-resistant strains of bacteria have resistance mutations that modify the chemical (cid:272)o(cid:373)positio(cid:374) of a(cid:374) a(cid:374)ti(cid:271)ioti(cid:272)"s target (e. g. , a (cid:373)e(cid:373)(cid:271)ra(cid:374)e protei(cid:374), a ri(cid:271)oso(cid:373)al rna, a (cid:272)o(cid:373)po(cid:374)e(cid:374)t of the cell wall). Because of the fitness costs, one would imagine that in the absence of antibiotics, resistant strains would decrease in frequency, and this is sometimes the case. However, as illustrated in the next slide, resistant strains often remain at high frequencies even in the absence of antibiotics. The main reason for this is compensatory mutations. What is a compensatory mutation? do not reduce the degree of resistance, but do reduce or eliminate the fitness costs associated with the resistant phenotype. Given that bacteria are haploid, and using r for resistant and r for sensitive at one locus, and c for compensated and c for uncompensated at another locus, a bacterial cell can be:
