The Questions of Developmental Biology

Further studies have strengthened the view that
the product of the wild-type bicoid gene is the
morphogen that controls anterior development.
First, bicoid is a maternal effect gene.
Messenger RNA from the mother's bicoid
genes is placed in the embryo by the mother's
ovarian cells (Figure 9.13; Frigerio et al. 1986;
ABerleth et al. 1988).
The bicoid RNA is strictly localized in the anterior portion of the oocyte (Figure 9.13B), where
the anterior cytoskeleton anchors it through the message's 3´ untranslated region (Ferrandon et al.
1997; Macdonald and Kerr 1998). This mRNA is dormant until fertilization, at which time it
receives a longer polyadenylate tail and can be translated. Driever and Nüsslein-Volhard (1988b)
have shown that when Bicoid protein is translated from this RNA during early cleavage, it forms
a gradient, with the highest concentration in the anterior of the egg and the lowest in the posterior
third of the egg. Moreover, this protein soon becomes concentrated in the embryonic nuclei in the
anterior portion of the embryo (Figure 9.13C-D; see also Figure 5.35).
Further evidence that Bicoid protein is the anterior morphogen came from experiments
that altered the steepness of the gradient. Two genes, exuperantia and swallow, are responsible
for keeping the bicoid message at the anterior pole of the egg. In their absence, the bicoid
message diffuses farther into the posterior of the egg, and the gradient of Bicoid protein is less
steep (Driever and Nüsslein-Volhard 1988a). The phenotype produced by these two mutants is
similar to that of bicoid-deficient embryos, but less severe. These embryos lack their most
anterior structures and have an extended mouth and thoracic region. Thus, by altering the gradient
of Bicoid protein, one correspondingly alters the fate of the embryonic regions.