The role of the sog gene in dorsal-ventral patterning of Drosophilaby
|
20 genes are responsible for development of the dorsal-ventral axis. Mutations in these genes result in abnormal or failed development of polarization in the Drosophila embryo.
Nusslein-Volhard's experiments in 1979 identified and characterized all
mutant alleles that affected the dorsal-ventral axis. Genes affecting dorsal-ventral
polarization fall into two categories:
1. Maternal Effect Genes-expressed during oogenesis
2. Zygotic Genes- expressed in the embryo
Maternal Effect genes are also known as egg-shape genes because of their
influence on the shape of the egg and shell. Dorsal-ventral polarization
is initiated by microtubule-dependent translocation of the oocyte nucleus.
Dorsal-ventral axis formation depends on:
1. Prior polarization of the anterior-posterior axis to establish the polarized
microtubule cytoskeleton.
2. Gene signaling triggering dorsalization and ventralization.
3. Co-operation of follicle and germ line cells in receiving and processing
signals.
Dorsal-ventral polarization is initiated in oogenesis, but is not irreversible
as further development continues in the embryo. The path of development
may be altered via injection of cytoplasmic gene products before entry into
the cellular blastoderm stage.
Holley et al. (1995) performed various experiments that elucidated the function of sog - a zygotic gene in Drosophila. They went on to find that there exists a conserved system for dorsal-ventral patterning in insects and vertebrates that involves sog and the Xenopus gene chordin.
Dorsal-ventral patterning within the ectoderm of the Drosophila embryo requires seven zygotic genes including sog (short gastrulation). Sog is expressed in the ventrolateral region of the embryo that gives rise to the nerve cord. Functionally, it is homologous to the chordin gene of Xenopus, which is expressed in the dorsal lip of the blastopore and in the dorsal mesoderm, in particular the notochord. They showed by injections of messenger RNA that both sog and chordin can promote ventral development in Drosophila, and that sog, like chordin, can promote dorsal development in Xenopus.
In Drosophila, sog antagonizes decapentaplegic (dpp),
which is a member of TGF-ß family and promotes dorsalization. In Xenopus,
a homologue of decapentaplegic is bmp-4, which promotes ventral development.
Results showed that mRNA injection of either sog or chordin
can produce ventral development in Drosophila. Sog or chordin
can produce dorsal development in Xenopus. This indicates molecular
conservation of the dorsal-ventral patterning mechanism during evolution
and links insects to vertebrates. However, their first experiments focused
on sog, specifically.
Loss of sog leads to a partial decrease in ventral neurogenic ectoderm
with increase in dorsal ectoderm. To test the capacity of sog to
form ectopic ventral structures in Drosophila embryos, synthetic
sog mRNA was injected dorsally.
This injection resulted in blocked differentiation of amnioserosal cells
(most dorsal pattern element). 47% of injected embryos resulted in patches
of ventral denticles on their dorsal sides. Many of these injected embryos
also lacked dorsally- or dorsolaterally-derived structures of the head and
tail; the anterior maxillary sense organs were missing in 95% of embryos,
and the posterior filzkorper were missing in 41% of embryos.
The next experiment involved females homozygous for the null allele dorsal (dl ); these flies lack Dorsal protein and do not express any ventral-specific genes. Their cuticle consists of only the most dorsal pattern elements. Injection of mRNA resulted in dorsolaterally-derived structures.
Therefore, sog transformed dl embryos from DO (dorsalized) phenotype to Dorsolateral phenotypes. Why did this happen? Sog could directly block decapentaplegic activity, or sog could encode a growth factor with activity independent of decapentaplegic.
The researchers think that specification of the neurogenic ectoderm requires
the action of one or more genes in addition to sog that are expressed
under dorsal control in the ventral regions of the embryo.
Holley et al. then attempted to correlate the activity of sog
to the activity of chordin in Xenopus.
sog mRNA injected into the ventral marginal region of Xenopus
embryos at the 4- to 16-cell stage caused a second blastopore lip to develop.
Then, they tried injection of chordin into Drosophila. Although
chordin mRNA had no effect, they found that injection of a chimeric
transcript encoding a chimaeric protein containing N-term region of sog
protein fused to mature chordin protein caused ventralization, although
it was much less active than sog. Furthermore, these results suggest
that the initial failure of chordin mRNA to ventralize Drosophila
embryos was due to inefficient secretion or improper processing of the chordin
protein in Drosophila.
In summary, the sog gene in Drosophila embryos is responsible for ventrolateral patterning and the development of the nerve cord. Its functional similarity to the chordin gene in Xenopus suggests that other similarities exist between the development of insects and vertebrates. Thus, Drosophila studies have again proven useful and relevant for studies of higher life forms.
DROSOPHILA |
XENOPUS |
sog |
chordin |
gives rise to nerve cord; |
expressed in dorsal blastopore lip & dorsal mesoderm & notochord |
dpp |
bmp-4 |
expressed dorsally, promotes dorsal development |
expressed ventrally, promotes ventral development |
Holley, S.A., Jackson, P.D., Sasal, Y., Lu, B., De Robertis, E.M., Hoffmann, F.M. and Ferguson, E.L. 1995. A conserved system for dorsal-ventral patterning in insects and vertebrates involving sog and chordin. Nature 376: 249-253.
| Gametogenesis | |||||
| The Foundations of Developmental Biology | |
The Developmental Biology Journal Club | |||
Copyright © 1996 Kristian Gordos, Tim Hunter, Monique Jericho,
and Arrany Khuong.This material may be reproduced for educational purposes
only provided credit is given to the original source.
October 28, 1996