<p style="text-align: justify;">Transgenic cotton Event-1 was developed through specific genetic modifications to be resistant to major caterpillar pests of cotton, including <i>Helicoverpa armigera</i> (American Bollworm), <i>Pectinophora gossypiella</i> (Pink Bollworm) and <i>Earis vittella</i> (Spotted Bollworm). Event-1 express a modified gene (<i>cry1Ac</i>) that encodes an insecticidal crystalline Cry1Ac delta-endotoxin protein, derived from the soil bacterium <i>Bacillus thuringiensis</i> subsp. <i>kurstaki</i> strain HD73. Insecticidal activity is caused by the selective binding of Cry1Ac protein 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 and eventual death due to bacterial sepsis. Delta-endotoxins, such as the Cry1Ac protein expressed in cotton Event-1, exhibit highly selective insecticidal activity against a narrow range of lepidopteran insects. The 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 non-lepidopteran insect guts or 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>nptII</i>) encoding the enzyme neomycin phosphotransferase II (NPTII), which inactivates aminoglycoside antibiotics such as kanamycin and neomycin, was also introduced into the genome of Event-1. 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>nptII</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.</p>
