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Development 134 (13): 2407-2414

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

Ronald J. Krieser1, Finola E. Moore1, Douglas Dresnek1, Brett J. Pellock1, Reena Patel1, Albert Huang1, Carrie Brachmann2, and Kristin White1,*

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.

* Author for correspondence (e-mail: kristin.white{at}cbrc2.mgh.harvard.edu)

Accepted for publication 11 April 2007.

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.

Key Words: Phosphatidylserine • Engulfment • Apoptosis • Drosophila


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