UNIT -5 DEVELOPMENTAL BIOLOGY (GURKEN PROTEIN )VERY VERY IMPORTANT TOPIC

The gurken gene of Drosophila melanogaster encodes a protein with homology to the transforming growth factor alpha (TGF-a) class of signaling molecules.

During Drosophila oogenesis, the gurken gene is transcribed in the cells of the germline. The gurken messenger RNA accumulates in the oocyte and is translated throughout oogenesis. The Gurken protein is transported to the oocyte membrane, and activates the Drosophila epidermal growth factor receptor (Egfr, tyrosine kinase receptor which is expressed on the adjacent follicle cells that surround the oocyte. The activation of this major transmembrane receptor regulates the expression of a number of genes in the follicle cells, and thus initiates a series of events that lead to the correct patterning of both the anteroposterior and the dorsoventral axis of the egg and embryo.

(1). Gurken acts as a ligand that is specific to oogenesis. The Gurken protein consists of an extracellular domain, which harbors a single epidermal growth factor (EGF)-like domain, a transmembrane domain, and a short cytoplasmic domain

 (2). It is homologous to the gene spitz of Drosophila, which acts as ligand of Egfr in the embryo and in imaginal discs.

Early in oogenesis, gurken mRNA is found in the developing oocyte, and the Gurken protein accumulates in the oocyte membrane. At this stage, the oocyte occupies only a small part of the volume of the egg chamber, and therefore only a limited number of follicle cells at the posterior of the egg chamber are in contact with the oocyte membrane. In this group of follicle cells, the Egfr is activated by Gurken protein, which results in the specification of these follicle cells as posterior cells. 

If  Gurken protein is absent, and the follicle cells at the posterior end of the egg chamber are not induced to assume a posterior cell fate. They consequently develop as anterior follicle cells, which results in the production of an egg with two anterior ends. The posterior follicle cells normally send a signal back to the oocyte, which organizes the cytoskeleton of the oocyte and specifies the posterior end of the oocyte. In the mutant egg chambers, no such signal is sent from the follicle cells, and the cytoskeleton of the oocyte is misorganized. RNAs such as bicoid or oskar, which should normally be localized to one end of the egg RNA localization are mislocalized in these mutant oocytes, and the embryos that develop inside such eggs have an abnormal antero-posterior pattern .

In midoogenesis -The oocyte has grown .The gurken RNA accumulates in the region around the oocyte nucleus, and the Gurken protein is now found in a very restricted part of the oocyte membrane, directly overlying the oocyte nucleus. At this stage, Gurken activates the Egfr in the lateral follicle cells that contact the oocyte on the side where the nucleus is situated. Activation of the Egfr in these lateral follicle cells induces them to become dorsal follicle cells. In the absence of gurken signaling, the lateral follicle cells develop into ventral follicle cells . The ventral follicle cells normally regulate the production of a ventral signal that activates the Toll receptor protein on the ventral side of the egg and is responsible for inducing ventral cell fates in the developing embryo. In the strong gurken mutants, therefore, the ventralization of the follicle cell epithelium leads to an overproduction of the ventral signal, and consequently to a ventralized embryo.

Gurken signaling presumably leads to the formation of a broad field of dorsal cell fates, but secondary patterning mechanisms appear to operate to lead to the final, complex pattern of cell fates of the mature egg. In addition, gurken signaling also interacts with signaling through decapentaplegic (dpp), a molecule with homology to TGF-b. In follicle cells that receive both the gurken signal and the dpp signal, formation of dorsal appendages is repressed, and formation of operculum cell fate is induced . The regulation of the embryonic ventral signal by activation of Egfr seems, however, to be independent of the production of dorsal anterior follicle cell fates. In situations where ectopic activation of Egfr in follicle cells is induced in parts of the follicle cell epithelium, embryos result that show only regional dorsalization, corresponding to the region of the follicle cell epithelium where Egfr was ectopically activated .

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