Understanding the Role of Gap Junction Mediated Cellular Communication in Cell Death and Cell Migration: Lessons from Drosophila Oogenesis

Acharjee, Sayan (2026) Understanding the Role of Gap Junction Mediated Cellular Communication in Cell Death and Cell Migration: Lessons from Drosophila Oogenesis. PhD thesis, Indian Institute of Science Education and Research Kolkata.

Text (PhD thesis of Sayan Acharjee (20RS029)) 20RS029.pdf - Submitted Version Restricted to Repository staff only Download (4MB)

Abstract

Morphogenesis in metazoans is associated with coordinated cellular activities. Signalling through autocrine, paracrine, and juxtacrine pathways, along with mechanical cues from adherens and tight junctions, ensures coordinated cellular behaviours in fundamental processes of morphogenesis, such as cell proliferation, migration, and cell death. Gap Junctions (GJs) play a key role by directly transferring ions and small molecules between cells, enabling synchronized responses between connected cells. My study focuses on GJ-mediated communication in two critical morphogenetic events: developmental cell death and collective cell migration. In the first part of my study, I investigated the role of Gap Junction (GJ)-mediated signalling in developmental cell death, focusing on phagoptosis—a non-apoptotic mechanism where living cells are engulfed and eliminated. Using Drosophila oogenesis, I examined how somatic follicle cells (SFCs) clear large germline nurse cells (NCs) to assist in egg maturation. This clearance is essential for ensuring egg fertility in the final stages of oogenesis. I found that the GJ protein Innexin 2 (Inx2) in SFCs is critical for NC elimination, and its channel function is necessary. Furthermore, elevating intracellular calcium levels in Inx2-deficient SFCs restored normal NC elimination, suggesting that calcium signalling downstream of Inx2 mediates the clearance of nurse cells by overlying follicle cells. I further show that calcium-dependent activation of CaMKII regulates Rac1 activity, promoting actin dynamics in SFCs. This in turn facilitates acidification and nuclear disintegration of NCs, enabling their engulfment. These findings reveal a novel mechanism by which GJ-mediated calcium signaling coordinates cellular cannibalism during oogenesis. In the second part of my study, I examined the role of gap junction (GJ)-mediated communication in collective cell migration, using the Drosophila border cell (BC) model during oogenesis. I found that Innexin 3 (Inx3) is crucial for efficient migration of the border cell cluster. Through live imaging, genetics, and immunohistochemistry, I showed that Inx3 maintains apical-basal polarity, essential for directed movement. These findings highlight a novel role for GJs in regulating polarity and mediating collective cell movement of border cells in Drosophila oogenesis.

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