Flies put the buzz back into long-term-potentiation

Two new papers show that an atypical protein kinase C may mediate the maintenance of long-term potentiation in the mouse hippocampus and of associative memory in Drosophila

WntD is a feedback inhibitor of Dorsal/NF-kappa B in Drosophila development and immunity

Regulating the Nuclear factor-κB (NF-κB) family of transcription factors is of critical importance to animals, with consequences of misregulation that include cancer, chronic inflammatory diseases, and developmental defects1. Studies in Drosophila melanogaster have proved fruitful in determining the signals used to control NF-κB proteins, beginning with the discovery that the Toll-NF-κB pathway, in addition to patterning the dorsal-ventral (D/V) axis of the fly embryo, defines a major component of the innate immune response in both Drosophila and mammals2,3. Here, we characterize the Drosophila wntD (Wnt inhibitor of Dorsal) gene. We show that WntD acts as a feedback inhibitor of the NF-κB homolog Dorsal during both embryonic patterning and the innate immune response to infection. wntD expression is under the control of Toll-Dorsal signaling, and increased levels of WntD block Dorsal nuclear accumulation, even in the absence of the IκB homolog Cactus. The WntD signal is independent of the common Wnt signaling component Armadillo (β-catenin). By engineering a gene knockout, we show that wntD loss-of-function mutants have immune defects and exhibit increased levels of Toll-Dorsal signaling. Furthermore, the wntD mutant phenotype is suppressed by loss of zygotic dorsal. These results describe the first secreted feedback antagonist of Toll signaling, and demonstrate a novel Wnt activity in the fly