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  • 1
    Electronic Resource
    Electronic Resource
    Knockdown resistance (kdr) to DDT and pyrethroid insecticides maps to a sodium channel gene locus in the housefly (Musca domestica) (1993)
    Springer
    Molecular genetics and genomics 240 (1993), S. 17-22 
    Details
    ISSN: 1617-4623
    Keywords: Musca domestica ; Sodium channel gene ; Pyrethroids ; Knockdown resistance (kdr)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The voltage-sensitive sodium channel is generally regarded as the primary target site of dichlorodiphenyl-trichloro-ethane (DDT) and pyrethroid insecticides, and has been implicated in the widely reported mechanism of nerve insensitivity to these compounds. This phenomenon is expressed as knockdown resistance (kdr) and has been best characterised in the housefly where several putative alleles, including the more potent super-kdr factor, have been identified. We report the isolation of cDNA clones containing part of a housefly sodium channel gene, designated Msc, which show close homology to the para sodium channel of Drosophila (99% amino acid identity within the region of overlap). Using Southern blots of insect DNA, restriction fragment length polymorphisms (RFLPs) at the Msc locus were identified in susceptible, kdr and super-kdr housefly strains. These RFLPs showed tight linkage to resistance in controlled crosses involving these strains, thus providing clear genetic evidence that kdr, and hence pyrethroid mode of action, is closely associated with the voltage-sensitive sodium channel.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00276878
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Identification of mutations in the housefly para-type sodium channel gene associated with knockdown resistance (kdr) to pyrethroid insecticides (1996)
    Springer
    Molecular genetics and genomics 252 (1996), S. 51-60 
    Details
    ISSN: 1617-4623
    Keywords: Key words Knockdown resistance (kdr) ; Musca domestica ; para ; Pyrethroid ; Sodium channel gene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract We report the isolation of cDNA clones containing the full 6.3-kb coding sequence of the para-type sodium channel gene of the housefly, Musca domestica. This gene has been implicated as the site of knockdown resistance (kdr), an important resistance mechanism that confers nerve insensitivity to DDT and pyrethroid insecticides. The cDNAs predict a polypeptide of 2108 amino acids with close sequence homology (92% identity) to the Drosophila para sodium channel, and around 50% homology to vertebrate sodium channel. Only one major splice from of the housefly sodium channel was detected, in contrast to the Drosophila para transcript which has been reported to undergo extensive alternative splicing. Comparative sequence analysis of housefly strains carrying kdr or the more potent super-kdr factor revealed two amino acid mutations that correlate with these resistance phenotypes. Both mutations are located in domain II of the sodium channel. A leucine to phenylalanine replacement in the hydrophobic IIS6 transmembrane segment was found in two independend kdr strains and six super-kdr strains of diverse geographic origin, while an additional methionine to threonine replacement within the intracellular IIS4-S5 loop was found only in the super-kdr strains. Neither mutation was present in five pyrethroid-sensitive strains. The mutations suggest a binding site for pyrethroids at the intracellular mouth of the channel pore in a region known to be important for channel inactivation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004389670006
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Identification of mutations in the houseflypara-type sodium channel gene associated with knockdown resistance (kdr) to pyrethroid insecticides (1996)
    Springer
    Molecular genetics and genomics 252 (1996), S. 51-60 
    Details
    ISSN: 1617-4623
    Keywords: Knockdown resistance (kdr) ; Musca domestica ; para ; Pyrethroid ; Sodium channel gene
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract We report the isolation of cDNA clones containing the full 6.3-kb coding sequence of thepara-type sodium channel gene of the housefly,Musca domestica. This gene has been implicated as the site of knockdown resistance (kdr), an important resistance mechanism that confers nerve insensitivity to DDT and pyrethroid insecticides. The cDNAs predict a polypeptide of 2108 amino acids with close sequence homology (92% identity) to theDrosophila para sodium channel, and around 50% homology to vertebrate sodium channels. Only one major splice form of the housefly sodium channel was detected, in contrast to theDrosophila para transcript which has been reported to undergo extensive alternative splicing. Comparative sequence analysis of housefly strains carryingkdr or the more potentsuper-kdr factor revealed two amino acid mutations that correlate with these resistance phenotypes. Both mutations are located in domain II of the sodium channel. A leucine to phenylalanine replacement in the hydrophobic IIS6 transmembrane segment was found in two independentkdr strains and sixsuper-kdr strains of diverse geographic origin, while an additional methionine to threonine replacement within the intracellular IIS4-S5 loop was found only in thesuper-kdr strains. Neither mutation was present in five pyrethroid-sensitive strains. The mutations suggest a binding site for pyrethroids at the intracellular mouth of the channel pore in a region known to be important for channel inactivation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02173204
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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