Evolution__3rd_Edition

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Figure 5.8
The mortality of mosquitos
(Culex quinquifasciatus) of
three genotypes at a locus
when exposed to various
concentrations of permethrin.
The susceptible homozygote
(SS) dies at lower
concentrations of the poison
than the resistant homozygote
(RR). The heterozygote (RS)
has intermediate resistance.
Redrawn, by permission of the
publisher, from Taylor (1986).
The real genetics of resistance is
known in some cases
The theory has practical
applications
Mortality (%)
98
95
90
80
70
60
50
40
30
20
CHAPTER 5 / The Theory of Natural Selection 117
SS RS RR
10
5
2
0.0001 0.001 0.01
NRDC 167 concentration (ppm)
0.1 1.0
recurrently, for 8.25 and 4.5 generations in this case, to give an average fitness for the
genotypes through the period. It appears that in Figure 5.7 the resistant mosquitoes had
about twice the fitness of the susceptible ones a which is very strong selection.
The genetics of resistance in this case are not known, and the one-locus, two-allele
model is an assumption only; but they are understood in some other cases. Resistance is
often controlled by a single resistance allele. For example, Figure 5.8 shows that the
resistance of the mosquito Culex quinquifasciatus to permethrin is due to a resistance
(R) allele, which acts in a semidominant way, with heterozygotes intermediate between
the two homozygotes. In houseflies, resistance to DDT is due to an allele called kdr. kdr
flies are resistant because they have fewer binding sites for DDT on their neurons. In
other cases, resistance may be due not to a new point mutation, but to gene amplification.
Culex pipiens, for instance, in one experiment became resistant to an organophosphate
insecticide called temephos because individuals arose with increased numbers of
copies of a gene for an esterase enzyme that detoxified the poison. In the absence of
temephos, the resistance disappeared, which suggests that the amplified genotype has
to be maintained by selection. A number of mechanisms of resistance are known, and
Table 5.8 summarizes the main ones that have been identified.
When an insect pest has become resistant to one insecticide, the authorities often
respond by spraying it with another insecticide. The evolutionary pattern we have seen
here then usually repeats itself, and on a shorter timescale. On Long Island, New York,
for example, the Colorado potato beetle (Leptinotarsa septemlineata) was first attacked
with DDT. It evolved resistance to it in 7 years. The beetles were then sprayed with
azinphosmethyl, and evolved resistance in 5 years; next came carbofuran (2 years),
pyrethroids (another 2 years), and finally pyrethroids with synergist (1 year). The
decreasing time to evolve resistance is probably partly due to detoxification mechanisms
that work against more than one pesticide. Pesticides cost money to develop, and
the evolution of resistance reduces the economic lifetime of a pesticide. Box 5.2 looks at
how the lifetime of a pesticide may be lengthened by slowing the evolution of resistance.
Insecticide resistance matters not only in the prevention of disease, but also in farming.
Insect pests at present destroy about 20% of world crop production, and it has been
estimated that in the absence of pesticides as much as 50% would be lost. Insect pests