Aminophospholipid translocase TAT-1 promotes phosphatidylserine exposure during C. elegans apoptosis.
Curr Biol
; 17(11): 994-9, 2007 Jun 05.
Article
in En
| MEDLINE
| ID: mdl-17540571
ABSTRACT
Phospholipids are distributed asymmetrically across the plasma-membrane bilayer of eukaryotic cells Phosphatidylserine (PS), phosphatidylethanolamine, and phosphoinositides are predominantly restricted to the inner leaflet, whereas phophatidylcholine and sphingolipids are enriched on the outer leaflet [1, 2]. Exposure of PS on the cell surface is a conserved feature of apoptosis and plays an important role in promoting the clearance of apoptotic cells by phagocytosis [3]. However, the molecular mechanism that drives PS exposure remains mysterious. To address this issue, we studied cell-surface changes during apoptosis in the nematode C. elegans. Here, we show that PS exposure can readily be detected on apoptotic C. elegans cells. We generated a transgenic strain expressing a GFPAnnexin V reporter to screen for genes required for this process. Although none of the known engulfment genes was required, RNAi knockdown of the putative aminophospholipid transporter gene tat-1 abrogated PS exposure on apoptotic cells. tat-1(RNAi) also reduced the efficiency of cell-corpse clearance, suggesting that PS exposure acts as an "eat-me" signal in worms. We propose that tat-1 homologs might also play an important role in PS exposure in mammals.
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Database:
MEDLINE
Main subject:
Phosphatidylserines
/
Cell Membrane
/
Caenorhabditis elegans
/
Apoptosis
/
Caenorhabditis elegans Proteins
/
Phospholipid Transfer Proteins
Limits:
Animals
Language:
En
Year:
2007
Type:
Article