Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.
Science Policy Alerts

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

Science 25 April 2008:
Vol. 320. no. 5875, pp. 528 - 531
DOI: 10.1126/science.1155847

Reports

Role of C. elegans TAT-1 Protein in Maintaining Plasma Membrane Phosphatidylserine Asymmetry

Monica Darland-Ransom,1 Xiaochen Wang,1* Chun-Ling Sun,1* James Mapes,1 Keiko Gengyo-Ando,2 Shohei Mitani,2 Ding Xue1{dagger}

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.

1 Department of Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 80309, USA.
2 Department of Physiology, Tokyo Women's Medical University School of Medicine and Core Research for Embryonic Science and Technology (CREST), Japan Science and Technology Agency (JST), Tokyo, 162-8666, Japan.

* These authors contribute equally to this work.

{dagger} To whom correspondence should be addressed. E-mail: ding.xue{at}colorado.edu

Read the Full Text






ADVERTISEMENT
Click Me!

ADVERTISEMENT
Click Me!

To Advertise     Find Products


Science. ISSN 0036-8075 (print), 1095-9203 (online)