Microbial infection activates two distinct intracellular signaling cascades in the immune aspects of the Drosophila fat. Gram-positive bacteria and fungi, mainly cause the call signaling path, while Gram-negative bacteria activate the Imd path. Loss of function mutants in any way reduce the resistance of the respective infections. Genetic screens was discovered a number of genes involved in purchase strattera these intracellular signaling cascades and how they appear in the microbial infection is largely unknown. Activation of transmembrane receptor Toll requires proteolytic cleaved form of extracellular cytokines like polypeptide, Sptzle, assuming that the call itself does not work as >> << bona fide recognition receptor of microbial patterns. This apparent contrast to mammals, Toll-like receptors >> << and raises the question of which host molecules actually recognize microbial models to activate the call through Sptzle. Here we present a mutation that blocks activation fee gram-positive bacteria and significantly reduces the resistance to this type of infection. Mutation
Zemmelveys (seml) inactivates the gene encoding the peptidoglycan recognition protein (PGRP-SA). Interestingly,
seml not affect the activation fee fungal infection, indicating the existence of different recognition systems for fungi to activate the call path. .
