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    <titleInfo>
      <title>Evidence of introgression of the ace-1(R) mutation and of the ace-1 duplication in West African# Anopheles gambiae$ s. s.</title>
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    <name type="personnal">
      <namePart type="family">Djogbénou</namePart>
      <namePart type="given">Luc</namePart>
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    <name type="personnal">
      <namePart type="family">Chandre</namePart>
      <namePart type="given">Fabrice</namePart>
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      <affiliation>IRD</affiliation>
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      <namePart type="family">Berthomieu</namePart>
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      <affiliation>IRD</affiliation>
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      <affiliation>IRD</affiliation>
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      <namePart type="family">Koffi</namePart>
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      <namePart type="family">Alout</namePart>
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    <name type="personnal">
      <namePart type="family">Weill</namePart>
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    <abstract>Background: The role of inter-specific hybridisation is of particular importance in mosquito disease vectors for predicting the evolution of insecticide resistance. Two molecular forms of Anopheles gambiae s.s., currently recognized as S and M taxa, are considered to be incipient sibling species. Hybrid scarcity in the field was suggested that differentiation of M and S taxa is maintained by limited or absent gene flow. However, recent studies have revealed shared polymorphisms within the M and S forms, and a better understanding of the occurrence of gene flow is needed. One such shared polymorphism is the G119S mutation in the ace-1 gene (which is responsible for insecticide resistance); this mutation has been described in both the M and S forms of A. gambiae s.s. Methods and Results: To establish whether the G119S mutation has arisen independently in each form or by genetic introgression, we analysed coding and non-coding sequences of ace-1 alleles in M and S mosquitoes from representative field populations. Our data revealed many polymorphic sites shared by S and M forms, but no diversity was associated with the G119S mutation. These results indicate that the G119S mutation was a unique event and that genetic introgression explains the observed distribution of the G119S mutation within the two forms. However, it was impossible to determine from our data whether the mutation occurred first in the S form or in the M form. Unexpectedly, sequence analysis of some resistant individuals revealed a duplication of the ace-1 gene that was observed in both A. gambiae s.s. M and S forms. Again, the distribution of this duplication in the two forms most likely occurred through introgression. Conclusions: These results highlight the need for more research to understand the forces driving the evolution of insecticide resistance in malaria vectors and to regularly monitor resistance in mosquito populations of Africa.</abstract>
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      <titleInfo>
        <title>Plos One</title>
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      <part>
        <detail type="volume">
          <number>3</number>
        </detail>
        <detail type="volume">
          <number>5</number>
        </detail>
        <extent unit="pages">
          <list> e2172</list>
        </extent>
      </part>
      <originInfo>
        <dateIssued>2008</dateIssued>
      </originInfo>
      <identifier type="issn">1932-6203</identifier>
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    <identifier type="uri">https://www.documentation.ird.fr/hor/fdi:010048499</identifier>
    <identifier type="doi">10.1371/journal.pone.0002172</identifier>
    <identifier type="issn">1932-6203</identifier>
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      <url usage="primary display" access="object in context">https://www.documentation.ird.fr/hor/fdi:010048499</url>
      <url access="row object">https://horizon.documentation.ird.fr/exl-doc/pleins_textes/divers17-08/010048499.pdf</url>
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      <recordCreationDate encoding="w3cdtf">2010-02-08</recordCreationDate>
      <recordChangeDate encoding="w3cdtf">2017-09-06</recordChangeDate>
      <recordIdentifier>fdi:010048499</recordIdentifier>
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