Investigating the Role of Insulin Receptor (InR) in Border cell Migration In Drosophila Oogenesis

Nisaa, Khairun (2015) Investigating the Role of Insulin Receptor (InR) in Border cell Migration In Drosophila Oogenesis. Masters thesis, Indian Institute of Science Education and Research Kolkata.

PDF (MS dissertation of Khairun Nisaa) Khairun_Nisaa_13IP008.pdf - Submitted Version Restricted to Repository staff only Download (1MB)

Abstract

Morphogenesis plays a fundamental role in the development of a multicellular organism. It is a multistep process where cells change shape, divide, move and differentiate to give form to various developing tissues. Though all these cellular processes play a very important role in morphogenesis, the underlying molecular mechanism regulating these processes is far from clear. In Drosophila oogenesis, transition from previtellogenic to vitellogenic phase of oocyte development has emerged as an excellent model system for studying morphogenesis. In this study, we particularly focused on group cell movement where a cluster of 6-10 cells detach from the epithelial layer, invade the neighboring cells and migrate to the oocyte boundary. These cells are called the border cells and eventually they form a passage on the oocyte surface to facilitate sperm entry during fertilization. Insulin signaling is known to play a major role in the phase transition from previtellogenic to vitellogenic phase. As this transition occurs, at the same time when border cells starts to migrate we hypothesized that insulin signaling regulates border cell movement. To understand the role of insulin signaling in border cell migration we down regulated insulin receptor function by over expressing Dominant Negative construct against Insulin receptor (DnInr). Consistent with our hypothesis, we observed that over expression of the DnInr construct impedes border cell movement. To understand how Insulin signaling affects cluster movement, we evaluated the level and distribution of various gene products that are known to regulate border cell movement. Interestingly, we observed that the cell adhesion molecule cadherin was upregulated in clusters where Inr function was down-regulated. Further we carried out live cell imaging to compare the dynamics of migration of Inr deficient cluster over the wild type. Results so far suggest that Insulin signaling play a role regulating the cell adhesion between the cells of the moving cluster.

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