Publication Date:
2008-04-26
Description:
The asymmetrical distribution of phospholipids on the plasma membrane is critical for maintaining cell integrity and physiology and for regulating intracellular signaling and important cellular events such as clearance of apoptotic cells. How phospholipid asymmetry is established and maintained is not fully understood. We report that the Caenorhabditis elegans P-type adenosine triphosphatase homolog, TAT-1, is critical for maintaining cell surface asymmetry of phosphatidylserine (PS). In animals deficient in tat-1, PS is abnormally exposed on the cell surface, and normally living cells are randomly lost through a mechanism dependent on PSR-1, a PS-recognizing phagocyte receptor, and CED-1, which contributes to recognition and engulfment of apoptotic cells. Thus, tat-1 appears to function in preventing appearance of PS in the outer leaflet of plasma membrane, and ectopic exposure of PS on the cell surface may result in removal of living cells by neighboring phagocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Darland-Ransom, Monica -- Wang, Xiaochen -- Sun, Chun-Ling -- Mapes, James -- Gengyo-Ando, Keiko -- Mitani, Shohei -- Xue, Ding -- R01 GM59083/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):528-31. doi: 10.1126/science.1155847.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18436785" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
Animals, Genetically Modified
;
Apoptosis
;
Caenorhabditis elegans/cytology/genetics/*metabolism
;
Caenorhabditis elegans Proteins/genetics/*metabolism
;
Cell Membrane/*metabolism
;
Germ Cells/cytology/metabolism
;
Muscle Cells/cytology/metabolism
;
Neurons/cytology/metabolism
;
Phagocytosis
;
Phosphatidylserines/*metabolism
;
Phospholipid Transfer Proteins/genetics/*metabolism
;
RNA Interference
;
Recombinant Fusion Proteins/metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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