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The cotton line 281-24-236 was genetically engineered to resist
attack from Lepidopteran insect pests such as the tobacco budworm,
cotton bollworm, beet armyworm, and soybean looper. This insect
resistance is conferred by the cry1F gene, originally isolated from
the common soil bacterium Bacillus thuringiensis (Bt) var. aizawai.
The term Recipient organism refers to an organism (either already modified or non-modified) that was subjected to genetic modification, whereas Parental organisms refers to those that were involved in cross breeding or cell fusion.
Line: 'Germain's Acala GC510'
- Agrobacterium-mediated DNA transfer
Ubiquitin gene promoter
Phosphinothricin N-acetyltransferase gene
ORF25 PolyA Terminator sequence
Lepidopteran-resistant cotton, with insect resistance conferred by
the cry1F gene from the common soil bacterium Bacillus
thuringiensis (Bt) var. aizawai.
Coding sequences of Cry1F and pat genes altered for optimal
expression in plant cells. The Cry1F protoxin is a chimeric,
full-length δ-endotoxin comprised of the core toxin of Cry1F from
Bacillus thuringiensis var. aizawai strain PS81I and nontoxic
portions of Cry1Ca3 and Cry1Ab1 proteins. Together, the portions of
Cry1Ca3 and Cry1Ab1 that comprise the chimeric C-terminal domain
are approximately those removed by alkaline proteases during the
formation of the active Cry1F core toxin.
- Resistance to diseases and pests
- Lepidoptera (butterflies and moths)
The cry1F gene produces the insect control protein Cry1F, a
delta-endotoxin, in the plant tissues. Cry proteins, of which Cry1F
is only one, act by selectively binding to specific sites localized
on the lining of the midgut of susceptible insect species.
Following binding, pores are formed that disrupt midgut ion flow,
causing gut paralysis and eventual death due to bacterial sepsis.
Cry1F is insecticidal only when eaten by the larvae of lepidopteran
insects (moths and butterflies), and its specificity of action is
directly attributable to the presence of specific binding sites in
the target insects. There are no binding sites for delta-endotoxins
of B. thuringiensis on the surface of mammalian intestinal cells,
therefore, livestock animals and humans are not susceptible to