ABSTRACT

These potential hazards and benefits are affected by modifications (e.g., truncation and rearrangement of codons; see Schnepf et al. 1998) of the introduced toxin genes to code only for the synthesis of active toxins, or a portion of the toxins, rather than of nontoxic crystalline protoxins (Figure 8.1). Consequently, it will not be necessary for an organism that ingests the active toxins to have a high midgut pH (~10.5) for solubilization of the ICPs and specific proteolytic enzymes to cleave the protoxins into toxic subunits. Therefore, non-target insects and organisms in higher and lower trophic levels could be susceptible to the toxins, even if they do not have an alkaline gut pH and appropriate proteolytic enzymes. This leaves only the third of the three barriers that appear to be responsible for the host specificity of the ICPs: i.e., specific receptors for the toxins on the midgut epithelium that are often, but not always, present in larger numbers in susceptible larvae (e.g., Van Rie et al. 1990, Wolfersberger 1990, Garczynski et al. 1991).