Deltex positively regulates Toll signaling in a JNK independent manner in Drosophila.

Abstract

Toll pathway is the center for the function of immune system in both Drosophila and mammals. Toll pathway in Drosophila gets activated upon binding of the ligand Spätzle to the receptor, Toll, triggering a series of proteolytic cascade culminating into the activation of the NF-κB factors Dorsal and/or Dif (Dorsal-related immunity factor). Inappropriate activation of the Toll pathway is often associated with systemic inflammation phenotype in the absence of infection, and thus, it is important to understand the regulation of Toll signaling. Deltex (Dx) is a context-dependent regulator of Notch signaling and has been linked with cell-mediated immunity in the mammalian system lately. However, the unambiguous role of Dx in humoral and cell-mediated immunity is yet to be explored. Our study unravels the novel role of Dx in Toll pathway activation. Gain of function of dx in Drosophila larvae results in increased melanotic mass formation and increased lamellocyte production. Our results also reveal the nuclear accumulation of transcription factors Dorsal and Dif and expression of Toll-associated antimicrobial peptides (AMP) in Dx over-expression background. Further, we also tried to elucidate the role of Dx in JNK-independent Toll activation. Here we present Dx as a novel candidate in the regulation of Toll pathway.