In addition to its function in embryonic development dorsal is expressed in larval and adult fat body where its RNA expression is enhanced upon injury. Injury also leads to a rapid nuclear translocation of DL from the cytoplasm in fat body cells. The nuclear localization of DL during the immune response is controlled by the Toll signaling pathway, comprising gene products that participate in the intracellular part of the embryonic dorsoventral pathway. In mutants such as Toll or cactus, exhibiting melanotic tumor phenotypes, DL is constitutively nuclear. Furthermore, the melanotic tumor phenotype of Toll and cactus is not dl dependent.
Toll is subject to glycosylation.
A constitutively activated mutant receptor, Toll10B, is processed into a distinct isoform of slower electrophoretic mobility when compared with the wild type molecule in cell lines and in the embryo. The wild type protein can also be processed into this form if over-expressed but in the embryo is present as the smaller species. The possible involvement of Toll in the Drosophila immune response was investigated by overexpressing Toll10B, a constitutively active mutant protein, in the Drosophila blood cell line mbn-2. Toll10B was found to increase CecA1 transcription. This effect depends on the presence of a kappa B-like site in the CecA1 promoter.