Genetics of Bt toxins and its Mode of action:
In the early 1980s, it was established that most genes coding for the ICPs reside on large 
transmissible plasmids, of which most are readily exchanged between strains by conjugation 
[44].Experimental data suggest that the C-terminal and middle domains 
of the toxin are involved in epithelial cell receptor binding and structural functions, while the 
N-terminal domain is primarily involved in ion channel and pore formation[56].and can be summarized in the following stages: 1) ingestion of sporulated Bt and ICP by an 
insect larva; 2) solubilization of the crystalline ICP in the midgut; 3) activation of the ICP by 
proteases; 4) binding of the activated ICP to specific receptors in the midgut cell membrane; 
5) insertion of the toxin in the cell membrane and formation of pores and channels in the gut 
cell membrane, followed by destruction of the epithelial cells [53].In the midgut of the target 
larva the parasporal crystalline ICP is dissociated to the protoxin form, and the protoxin is
then activated to a biologically active holotoxin by the proteolytic enzymes and specifically 
the alkaline environment of the gut [55]..Since these initial studies, numerous ICP genes have been cloned, sequenced and used 
to construct Bt strains with novel insecticidal spectra [45].?-endotoxins are encoded by the 
Cry and Cyt genes These genes become active during sporulation because they are controlled 
by a dedicated RNA polymerase that is also synthesized specifically while spores areforming.Pore or ion 
channel formation occurs after the binding to the receptor and insertion of the N-terminal 
domain into the membrane, whereby the regulation of the transmembrane electric potential is
disturbed.