(Alliance, FBgn0262473 )

Receptor for the cleaved activated form of spz, spaetzle C-106 (PubMed:12872120). Binding to spaetzle C-106 activates the Toll signaling pathway and induces expression of the antifungal peptide drosomycin (PubMed:12872120, PubMed:8808632, PubMed:10973475). Component of the extracellular signaling pathway that establishes dorsal-ventral polarity in the embryo (PubMed:3931919). Promotes heterophilic cellular adhesion (PubMed:2124970). Involved in synaptic targeting of motoneurons RP5 and V to muscle 12 (M12); functions as a repulsive cue inhibiting motoneuron synapse formation on muscle 13 (M13) to guide RP5 and V to the neighboring M12, where its expression is repressed by tey (PubMed:20504957). May also function in embryonic neuronal survival and the synaptic targeting of SNa motoneurons (PubMed:19018662).

(UniProt, P08953)

Maternal expression of the Toll gene is required for the normal production and distribution of positional information in the embryo (Anderson et al., 1985); zygotic expression is required to maintain viability in early larvae (Gerttula et al., 1988). Toll mutants and deficiencies occurring in the mother result in lethal abnormalities in the pattern of gastrulation and the differentiation of cuticular structures in the offspring. When null alleles and deficiencies are homozygous in the zygote, delayed development and early lethality result. Females heterozygous for dominant Toll alleles are sterile, their lethal embryos being partially ventralized regardless of their genotype. Dorsoventral polarity is present; a furrow is formed in the midventral region, but the lateral cephalic fold is shifted to the dorsal side and the normal dorsal folds are missing. The cuticle lacks dorsal hairs, filzkorper, spiracles, head sensory organs, and a head skeleton; there are patches of denticles extending around the entire dorsoventral circumference of the embryo (Anderson et al., 1985a). The ventral nervous system is also expanded (Campos-Ortega, 1983). Embryos produced by females hemizygous for some dominant alleles (Tl1/Df; Tl3/Df) are ventralized, but the embryos of other hemizygotes (Tl2/Df; Tl4/Df) are dorsalized, all cells behaving at gastrulation and in differentiation like wild-type dorsal cells. In embryos derived from Tl/+ females, virtually the entire ectoderm capable of neurogenesis in response to absence of Dl function (Campos-Ortega, 1983, Wilhelm Roux's Arch. Dev. Biol. 192: 317-26). Whereas females heterozygous for recessive alleles of Tl are fertile, homozygous Tl-recessive females are viable but sterile, their lethal embryos lacking dorsoventral polarity and forming no ventral furrow at gastrulation. In most recessive alleles (Tlr5, Tlr6, Tlr7), the embryos are partially dorsalized with laterally derived structures (Anderson et al., 1985a); for example, Tlr6 embryos differentiate dorsal hairs, filzkorper, and ventral denticle bands of nearly normal width, but lack mesoderm (Anderson and Nusslein-Volhard, 1986). In one allele (Tlr4), however, embryos have no dorsal hairs and show rings of denticles as in TlD embryos (Anderson et al., 1985a). Hemizygotes for the Toll-recessives resemble the corresponding homozygotes in phenotype. A number of Toll alleles were obtained as reversions of the Toll-dominant phenotype (see table). When crossed to wildtype males, females heterozygous for a null-type reversion are fully fertile; however, when crossed to males who are also heterozygous for a Toll null, these females produce Tl-homozygotes who are zygotic lethals, dying as early larvae and producing no Toll transcript. Heteroallelic combinations of reversions such as Tlrv1/Tlrv2 produce sterile females with lethal dorsalized embryos. Females carrying combinations of certain reversions and Toll-dominant (or Toll-recessive) alleles produce embryos with phenotypes like those of Toll-dominant (or Toll-recessive) hemizygotes. Most of the reversions, when in trans to deficiencies, result in females with dorsalized embryos, but a few hemizygous reversion females (Tlrv21, Tlrv22, Tlrv23) produce ventralized embryos (Hashimoto et al., 1988). The lethal embryos of Df(3R)Tl-X/Df(3R)ro-XB3 (null) females (Hashimoto et al., 1988), are completely dorsalized, never making ventral furrows, filzkorper, or denticles; their germ bands fail to extend; no Toll transcript is produced in these embryos except when contributed by wild-type fathers (Gerttula et al., 1988). The 97D1-2 breakpoint of the Toll deficiency Df(3R)Tl-X maps within the 6.0 kb EcoRI fragment of a Toll clone (Hashimoto et al., 1988). Injection of wild-type cytoplasm into embryos of Toll-deficient females restores the wild-type dorsoventral pattern, the site of the injection determining the midventral part of the pattern (Anderson et al., 1985b); (also see molecular biology section).