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Hyperactive Rac converts sublethal to lethal trogocytosis in vivo
Lauren Penfield1, Abhinava K Mishra1,2, Morgan Smith1
1Molecular, Cellular, and Developmental Biology Department, University of California, Santa Barbara, CA 93106.
Summary
Hyperactivated Rac signaling in Drosophila border cells triggers lethal cannibalism of nurse cells. This study reveals mechanisms of cell killing and engulfment, with implications for cancer therapies.
Area of Science:
- Cell Biology
- Developmental Biology
- Molecular Biology
Background:
- The small GTPase Rac is crucial for cell shape, migration, and phagocytosis.
- Constitutively active Rac (RacG12V) induces cannibalism in Drosophila border cells.
Purpose of the Study:
- Investigate mechanisms of border cell-mediated killing of nurse cells.
- Elucidate the roles of Rac and Draper in trogocytosis.
Main Methods:
- Drosophila melanogaster model system.
- Clonal analysis of RacG12V expression.
- Assessing cell death markers (caspase activation, nuclear damage).
Main Results:
- RacG12V causes lethal 'bites' leading to nurse cell death and engulfment by follicle cells.
- Rac and Draper are essential for both sublethal and lethal trogocytosis.
- Rac-independent germline death can be induced by increased Draper or JNK activity.
Conclusions:
- Hyperactivated Rac in few cells can trigger destruction of a larger cell mass.
- Multiple pathways can activate border cells for killing.
- Findings inform the development of cancer-engulfing therapies (RaceCAR-Ms).
