Larvae of mosquitoes and black flies feed on small particulate matter present in their aquatic breeding habitats. Upon ingestion, the crystal proteins dissolve at the alkaline pH of the insect gut, proteolytic action releases toxic fragments, the epithelial cells of the gut swell and lyse, and death rapidly ensures. At the molecular level, the model for toxicity proposed by Knowles et al. has a large amount of experimental support. The processed toxin binds to a specific receptor, probably a glycoprotein, on the plasma membranes of susceptible cells in the midgut epithelium. This initial binding could account for the specificity of the toxin, and it follows that resistance to the toxin would result from structural changes in the receptor. Initial binding is followed by the creation of tiny pores in the membrane leading to colloid-osmotic lysis in which equilibration of ions across the pores leads to a net influx of ions, an accompanying influx of water, cell swelling, and lysis. Disruption of the epithelial lining kills the larvae rapidly. This model is based on the studies with the processed cytA protein, but the exact mechanism of action can account for the toxicity of other B. thuringiensis toxins.
Author(s) Details:
B. Usharani,
Department of Biomedical Genetics, Institute of Basic Medical Sciences, University of Madras, Tamil Nadu, India.
R. Venkateswari,
Department of Medical Microbiology, Institute of Basic Medical Sciences, University of Madras, Tamil Nadu, India.
P. Suganthi,
Department of Medical Biochemistry, Institute of Basic Medical Sciences, University of Madras, Tamil Nadu, India.
M. Muthuraj,
State TB Training and Demonstration Centre, Intermediate Reference Laboratory, Government Hospital for Chest Diseases, Puducherry, India.