<p style="text-align: justify;">Transgenic Russet Burbank potato lines BT6, BT10, BT12, BT16, BT17, BT18, and BT23 (trademark NewLeaf&trade; ), were bioengineered to be resistant to attack by Colorado potato beetle (CPB, <i>Leptinotarsa decemlineata</i> Say), a major insect pest of potatoes. These novel potato lines contain a CPB resistance gene (<i>cry3A</i>) that encodes an insecticidal crystalline Cry3A delta-endotoxin protein, derived from the soil bacterium <i>Bacillus thuringiensis</i> subsp. tenebrionis (B.t.t). Insecticidal activity is caused by the selective binding of Cry3A to specific sites localized on the brush border midgut epithelium of susceptible insect species. Following binding, cation-specific pores are formed that disrupt midgut ion flow and thereby cause gut paralysis, ultimately leading to bacterial sepsis and death. Delta-endotoxins, such as the Cry3A protein expressed in CPB resistant potato lines, exhibit highly selective insecticidal activity against a narrow range of coleopteran insects such as CPB, elm leaf beetle and yellow mealworm. Their specificity of action is directly attributable to the presence of specific receptors in the target insects. There are no receptors for delta-endotoxins of <i>B. thuringiensis</i> on the surface of mammalian intestinal cells, therefore, livestock animals and humans are not susceptible to these proteins.</p>

<p style="text-align: justify;">An antibiotic resistance marker gene (<i>neo</i>) encoding the enzyme neomycin phosphotransferase II (NPTII), which inactivates aminoglycoside antibiotics such as kanamycin and neomycin, was also introduced into the genome of these plants. This gene was derived from a bacterial transposon (Tn5 transposable element from <i>Escherichia coli</i>) and was included as a selectable marker to identify transformed plants during tissue culture regeneration and multiplication. The expression of the <i>neo</i> gene in these plants has no agronomic significance and the safety of the NPTII enzyme as a food additive was evaluated by the United States Food and Drug Administration in 1994 (US FDA, 1994).</p>
