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).
