www.czu.cz ; www.raupp.info

Researchers have identified that a specific point in the genetic code
appears not only to control an organism's resistance to a class of
pesticides but also to significantly influence the ability of an organism to
evolve such resistance at all. Identifying such specific and strong
constraints on short-term evolutionary change are likely to help ecologists
and public-health experts understand, and potentially predict, the ability
of particular species to quickly develop resistance to substances such as
insecticides. The new work also illuminates the kind of genetic technicality
that can shape evolution, July 2004 by Heidi Hardman .


The work, performed by an international team led by Mylene Weill of the
Université Montpellier II (France), concerned the ability of mosquito
species to develop resistance to two major classes of insecticides,
carbamates and organophosphates (OPs). Previous work had shown that a single
base-pair alteration, G119S, within the mosquito's version of the AchE1 gene
conferred high levels of resistance to these insecticides. Not all mosquito
species exposed to high levels of carbamates and OPs develop resistance,
however. For example, Anopheles gambiae, the mosquito vector for malaria, is
able to develop resistance in this way, whereas Aedes aegytpi, the vector
for yellow fever and dengue fever, has never developed high levels of
resistance.

The new study reveals the reason for this striking discrepancy in
adaptation. First, the researchers determined that the G119S version of the
Ae. aegypti AchE1 protein was indeed resistant to insecticide action in the
test tube, suggesting that the mutation would confer resistance to the
mosquito in principle but that for some reason the mutation does not appear
in Ae. aegypti populations. Looking more closely at the Ae. aegypti gene
sequence for AchE1 revealed the answer. The researchers found that in this
species, the three-letter DNA code at glycine position 119 is different from
that found in the other mosquitoes studied thus far. The difference is
"silent," that is, the gene still codes for the same amino acid at the 119
position. But it means - critically, as it turns out - that a single
mutation of the site cannot result in the G119S change needed for
resistance. In A. gambiae, it only takes one base mutation to alter the code
in the right way; in Ae. aegypti, it takes two adjacent base mutations - a
far less likely event.

The researchers went on to sequence the 119 position in 26 natural
populations of Ae. aegypti in 12 countries and found that in all cases the
three-letter codon at this position was the same, fitting with the lack of
AchE1-based resistance in this species observed worldwide. They also showed
that the "constrained" codon is present in 31 of 44 additional mosquito
species, almost all of which indeed appear to have failed to develop
resistance. Among those species with the codon version that easily mutates
to confer resistance, about 50% have already developed high AchE1-based
resistance. Most of the others are not insecticide-controlled.

[www.eurekalert.org]

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