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The entomopathogenBacillus sphaericusis an important tool for the vector control ofCulexsp., and its effectiveness has been validated in field trials. The appearance of resistance to this bacterium, however, remains a threat to its use, and attempts have been made to understand the resistance mech-anisms. | iFEBS Journal A second independent resistance mechanism to Bacillus sphaericus binary toxin targets its a-glucosidase receptor in Culex quinquefasciatus Tatiany Patricia Romao1 Karlos Diogo de Melo Chalegre1 Shana Key1 Constancia Flavia Junqueira Ayres1 Claudia Maria Fontes de Oliveira1 Osvaldo Pompilio de-Melo-Neto2 and Maria Helena Neves Lobo Silva-Filha1 1 Department of Entomology Centro de Pesquisas Aggeu Magalhâes Fundacao Oswaldo Cruz Recife-PE Brazil 2 Department of Microbiology Centro de Pesquisas Aggeu Magalhaes Fundacao Oswaldo Cruz Recife-PE Brazil Keywords Bacillus sphaericus binding site Culex quinquefasciatus a-glucosidase resistance Correspondence M. H. N. L. Silva-Filha Centro de Pesquisas Aggeu Magalhaes-Fiocruz Avenue Moraes Rego s n Cidade Universitaria Recife-PE Brazil50670-420 Tel 55 81 21012553 Fax 55 81 34532449 E-mail mhneves@cpqam.fiocruz.br Note Nucleotide sequence data has been submitted to the GenBank database under the accession number DQ333335. Received 15 December 2005 revised 27 January 2006 accepted 13 February 2006 doi 10.1111 j.1742-4658.2006.05177.x The entomopathogen Bacillus sphaericus is an important tool for the vector control of Culex sp. and its effectiveness has been validated in field trials. The appearance of resistance to this bacterium however remains a threat to its use and attempts have been made to understand the resistance mechanisms. Previous work showed that the resistance to B. sphaericus in a Culex quinquefasciatus colony is associated with the absence of the w 60-kDa binary toxin receptor in larvae midgut microvilli. Here the gene encoding the C. quinquefasciatus toxin receptor Cqm1 was cloned and sequenced from a susceptible colony. The deduced amino-acid sequence confirmed its identity as an a-glucosidase and analysis of the corresponding gene sequence from resistant larvae implicated a 19-nucleotide deletion as the basis for resistance. This deletion changes the ORF and originates a premature stop codon .
