Organs compose of various tissues that form a structural unit, which fulfills a particular function in our bodies. An impairment of organ development often results in abnormalities connected with loss of organ function or disease. Currently, it is not clear how exactly organs are formed and little is known about the molecular mechanisms underling their development. Basic research shows that the process of organ development is quite complex and involves a precise coordination among biological events such as cell polarity in epithelial tissues, communication among cells and also cell rearrangements/movements.

I am using Drosophila melanogaster (fruit fly) as a simple model organism to understand the principles that underlie the formation of organ shape. Drosophila provides an excellent model system for the study of such principles, as eggs undergo complex morphological changes, turning the initial spherical shape of an immature egg into the ellipsoid shape of a mature egg. The mature Drosophila egg arises from a structure called an egg chamber (the 'immature egg') and is composed of germ-line cells, which are covered with a somatic line called the follicle epithelium. Therefore, the egg chamber is often considered as a primitive organ.

The elongation process in Drosophila egg chambers is not fully understood. Up to now, a few cytoplasmatic proteins, components of extracellular matrix (ECM) and proteins providing cell-to-ECM or cell-to-cell communication have been implicated in this process. Planar cell polarity (PCP) of cytoskeletal structures at the basal side of follicle cells has been linked with the elongation of egg chambers. In addition, a recently discovered morphological process, involving a circumferential collective movement of follicle cells and the germ line around the longer egg chamber axis (also called a global rotation of egg chambers), has been correlated with the egg shape. However, it is unclear how exactly the PCP information is translated into the final shape of the Drosophila egg at the molecular level or what source initiates the PCP to break the egg chamber symmetry in early oogenesis. Currently, we know that the polarity information appears prior to the onset of global rotation, indicating a dependency of the global rotation on proper PCP cues. Nevertheless, it is puzzling as to what initiates and drives the global rotation and especially what function it has in the elongation process in Drosophila oogenesis.

I am particularly interested in the fat2 gene. It encodes one of the key PCP players, providing cell-to-cell communication among follicle cells, and its presence is essential for the global rotation in Drosophila egg chambers. I have previously tried to understand how the Fat2 protein functions in Drosophila oogenesis in the lab of Prof. Dr. Christian Dahmann. In Pavel's lab, I would like to continue with this work and would like to pursue the following questions:

1) What is the initial source that is responsible for the earliest symmetry breaking prior to the onset of the global rotation?

2) How does Fat2 propagate the polarity cue at the molecular level?

3) What is the function of the global rotation in respect to the elongation process?

4) Are these processes evolutionarily conserved?

I would also like to broaden the range of known genes, involved in 'shaping the egg', by carrying out a new screen and combining this with the latest FlyFos techniques.

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