The Drosophila homolog of the putative phosphatidylserine receptor functions to inhibit apoptosis

Author:

Krieser Ronald J.1,Moore Finola E.1,Dresnek Douglas1,Pellock Brett J.1,Patel Reena1,Huang Albert1,Brachmann Carrie2,White Kristin1

Affiliation:

1. Cutaneous Biology Research Center, Massachusetts General Hospital, 149 13th street, Charlestown, MA 02129, USA.

2. Developmental and Cell Biology Department, University of California, Irvine,5205 McGaugh Hall, Irvine, CA 92697, USA.

Abstract

Exposure of phosphatidylserine is a conserved feature of apoptotic cells and is thought to act as a signal for engulfment of the cell corpse. A putative receptor for phosphatidylserine (PSR) was previously identified in mammalian systems. This receptor is proposed to function in engulfment of apoptotic cells, although gene ablation of PSR has resulted in a variety of phenotypes. We examined the role of the predicted Drosophila homolog of PSR (dPSR) in apoptotic cell engulfment and found no obvious role for dPSR in apoptotic cell engulfment by phagocytes in the embryo. In addition, dPSR is localized to the nucleus, inconsistent with a role in apoptotic cell recognition. However, we were surprised to find that overexpression of dPSR protects from apoptosis, while loss of dPSR enhances apoptosis in the developing eye. The increased apoptosis is mediated by the head involution defective (Wrinkled) gene product. In addition, our data suggest that dPSR acts through the c-Jun-NH2 terminal kinase pathway to alter the sensitivity to cell death.

Publisher

The Company of Biologists

Subject

Developmental Biology,Molecular Biology

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