Novel genetic factors involved in resistance to Bacillus thuringiensis in Plutella xylostella.
The widespread and sustainable exploitation of the entomopathogen Bacillus thuringiensis (Bt) in pest control is threatened by the evolution of resistance. Although resistance is often associated with loss of binding of the Bt toxins to the insect midgut cells, other factors have been implicated. Here we used suppressive subtractive hybridization and gene expression suppression to identify additional molecular components involved in Bt-resistance in Plutella xylostella. We isolated transcripts from genes that were differentially expressed in the midgut of larvae from a resistant population, following ingestion of a Bt kurstaki HD1 strain-based commercial formulation (DiPel), and compared with a genetically similar susceptible population. Quantitative real-time polymerase-chain reaction (RT-PCR) analysis confirmed the differential basal expression of a subset of these genes. Gene expression suppression of three of these genes (P. xylostella cyclin-dependent kinase 5 regulatory subunit associated protein 1-like 1, stromal cell-derived factor 2-like 1 and hatching enzyme-like 1) significantly increased the pathogenicity of HD1 to the resistant population. In an attempt to link the multitude of factors reportedly influencing resistance to Bt with the well-characterized loss of toxin binding, we also considered Bt-resistance models in P. xylostella and other insects.
Environmental Biotechnology Group, Centre for Genetic Engineering and Biotechnology (CIGB), Havana, Cuba.
C
C
Ayra-Pardo
Division of Biology, Department of Life Sciences, Faculty of Natural Sciences, Imperial College London, Silwood Park Campus, Ascot, Berkshire, UK.
B
B
Raymond
Division of Biology, Department of Life Sciences, Faculty of Natural Sciences, Imperial College London, Silwood Park Campus, Ascot, Berkshire, UK.
A
A
Gulzar
Environmental Biotechnology Group, Centre for Genetic Engineering and Biotechnology (CIGB), Havana, Cuba.
L
L
Rodríguez-Cabrera
Environmental Biotechnology Group, Centre for Genetic Engineering and Biotechnology (CIGB), Havana, Cuba.
I
I
Morán-Bertot
School of Life Sciences, University of Sussex, Brighton, UK.
N
N
Crickmore
Division of Biology, Department of Life Sciences, Faculty of Natural Sciences, Imperial College London, Silwood Park Campus, Ascot, Berkshire, UK.
D J
DJ
Wright
D000818:Animals; D001413:Bacillus thuringiensis; D000083722:Bacillus thuringiensis Toxins; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism; D061046:Biological Control Agents; D004731:Endotoxins / Q000235:genetics / Q000378:metabolism; D041981:Gastrointestinal Tract / Q000378:metabolism; D015870:Gene Expression; D017344:Genes, Insect; D006460:Hemolysin Proteins / Q000235:genetics / Q000378:metabolism; D019476:Insect Proteins / Q000235:genetics / Q000378:metabolism*; D007305:Insecticide Resistance / Q000235:genetics*; D007814:Larva / Q000235:genetics / Q000378:metabolism; D009036:Moths / Q000235:genetics / Q000378:metabolism*
D000083722:Bacillus thuringiensis Toxins; D001426:Bacterial Proteins; D061046:Biological Control Agents; D004731:Endotoxins; D006460:Hemolysin Proteins; D019476:Insect Proteins; C030956:insecticidal crystal protein, Bacillus Thuringiensis
ABCC2; Bacillus thuringiensis, Plutella xylostella, Bt-resistance; RNAi; differential expression