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Animal cap
A
Vegetal pole
NO signal
signal
Isolated animal cap
mRNA for
truncated activin
receptor
B
Control
Experimental
oocyte
Intact
Dissociated
+BMP 4 &
Dissociate
blastula
isolated
animal
cap
Epidermis Epidermis
FIGURE 1.21 Dissociation of animal cap cells prior to gastrula-
tion causes most of them to differentiate into neurons in culture.
Animal caps can be cultured intact (left) or dissociated into single
cells by removing the Ca +2 ions from the medium (middle and right).
If the intact caps are put into culture, they develop as epidermis
(left). If the dissociated animal cap cells are cultured, they develop
into neurons (red; middle). This result supports the hypothesis that
the neural fate is actively suppressed by cellular associations in the
ectoderm. If the cells are dissociated and then BMP is added to the
culture dish, the cells do not become neurons, but instead act as if
they are not dissociated and develop as epidermis (right).
Neural tissue
neural tissue
FIGURE 1.20 Expression of a truncated activin receptor blocks
normal signaling through the receptor and induces neural tissue.
A. The normal activin receptor transmits a signal to the cell when
activin binds the receptor and it forms a dimer. The truncated activin
receptor still binds the activin (or related TGF-b), but now the
normal receptor forms dimers with the truncated receptor. Lacking
the intracellular domain to signal, the truncated receptor blocks
normal signal transduction through this receptor. B. Oocytes injected
with the truncated activin receptor develop to the blastula stage,
and when the animal caps were dissected from these embryos,
they developed into neural tissue without the addition of a neural
inducer. This result indicated that inhibiting this signaling pathway
might be how neural inducers function.
epidermis
tebrates and invertebrates (Figure 1.22). Analysis of
chordin's sequence revealed an interesting homology
with a Drosophila gene called short gastrulation or sog .
Sog is expressed in the ventral side of the fly embryo,
and mutations in this gene in Drosophila result in defec-
tive dorsal-ventral patterning of the embryo. In null
mutants of sog , the epidermis expands and the neuro-
genic region is reduced. And, like chordin, microinjec-
tion of sog into the nonneurogenic region of the
embryo causes the formation of ectopic neural tissue.
Thus, sog seems to be the functional homolog of
chordin. At this point the advantages of fly genetics
were important. From analysis of other Drosophila
mutants, it was possible to show that sog interacts with
a gene called decapentaplegic , or dpp , a TGF-like protein
related to the vertebrate genes known as bone-
morphogenic proteins, BMPs. Dpp and sog directly
antagonize one another in Drosophila. Mutations in dpp
have the opposite phenotype as sog mutations; in dpp
expressed in the organizer region of the embryo at the
time of neural induction, like chordin and noggin.
CONSERVATION OF
NEURAL INDUCTION
Even more fascinating than the identification of
three candidate neural-inducing factors in a relatively
short period of time is that these three factors may all
act by a related mechanism and that this mechanism
appears to be at least partially conserved between ver-
 
 
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