Monday, December 10, 2007 - 4:35 PM
0691

Does TMOF enhance the effect of Bti toxins on larval Aedes aegypti?

Dov Borovsky, dobo@mail.ifas.ufl.edu1, Annelies Laeremans, annelies.laeremans@gmail.com1, Vadim Khasdan, khasdan@bgumail.bgu.ac.il2, Eitan Ben-Dov, etn@bgu.ac.il2, and Arieh Zaritsky, ariehz@bgu.ac.il2. (1) University of Florida, FMEL, 200 9th St SE, Vero Beach, FL, (2) Ben Gurion University, Life Sciences, Be'er Sheva, Israel, Israel

TMOF, a mosquito decapeptide hormone (YDPAPPPPPP), is the physiological signal that terminates trypsin biosynthesis in adult and larval mosquito gut. Female mosquito produces the hormone in the ovary and secretes it into the hemolymph 24-48 h after the blood meal. The hormone binds a gut specific receptor and causes rapid decline in trypsin biosynthesis in the gut. Feeding larval mosquito recombinant cells producing the hormone stops trypsin biosynthesis, larval growth, causes anorexia and larval death. Bti toxins, on the other hand, are bacterial toxins that bind to the gut epithelial cells, produce pores, cause loss of osmotic pressure and death. To study a possible synergism between TMOF and Bti toxins, we have cloned and expressed TMOF in Pichia pastoris cells and Cry4Aa, Cry11Aa, Cyt2Aa and p-20 in E. coli cells. A second E. coli construct producing active Cry4Aa alone or fused to GST was also produced. Different concentrations of the bacterial and yeast cells were fed to larval Ae. aegypti to test for possible synergistic effect. Mosquito larvae that were starved by eating recombinant P. pastoris cells producing TMOF were highly sensitive to low concentrations of Bti toxins as compared with larvae that were fed non-recombinant P. pastoris cells and Bti toxins. The genetic engineering and the effect of TMOF and Bti toxins alone and in concert on mosquito larvae will be discussed.


Species 1: Diptera Culicidae Aedes Aedes aegypti (yellow fever mosquito)