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Little PIP, little PIP, let me in

Little PIP, little PIP, let me in <h2>Little PIP, little PIP, let me in</h2> PIP 2 (green) is eliminated by bacteria (pink) that express SigD (right). Grinstein/Macmillan In one simple hydrolysis step, bacteria make the plasma membrane squishy enough to ease invasion, according to new results from two groups. The groups studied different pathogens, but both came to similar conclusions. Both bacteria, Shigella and Salmonella , inject several invasion-promoting proteins into the host, including a protein with similarity to a mammalian inositol phosphatase. Mauricio Terebiznik, Sergio Grinstein (Hospital for Sick Children, Toronto, ON), and colleagues watched how phosphoinositides were affected during Salmonella infection. They found that one PIP 2 species, PtdIns(4,5)P 2 , was depleted from the base of membrane ruffles that formed where bacteria were pushing to get in, thanks to the phosphatase activity of the SigD effector protein. Like SigD, the Shigella effector IpgD studied by Kirsten Nieburh (Institut Pasteur, Paris, France), Bernard Payrastre (INSERM, Toulouse, France), and colleagues also removed PIP 2 from target cells; in this case, the product was identified as PtdIns(5)P. The result in both cases was a softer plasma membrane. Expression of either phosphatase in mammalian cells caused membrane blebbing and relaxed attachment between the actin cytoskeleton and http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Cell Biology Rockefeller University Press

Little PIP, little PIP, let me in

The Journal of Cell Biology , Volume 159 (2): 200 – Oct 28, 2002

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Publisher
Rockefeller University Press
Copyright
Copyright © 2002, by The Rockefeller University Press
ISSN
0021-9525
eISSN
1540-8140
DOI
10.1083/jcb1592rr3
Publisher site
See Article on Publisher Site

Abstract

<h2>Little PIP, little PIP, let me in</h2> PIP 2 (green) is eliminated by bacteria (pink) that express SigD (right). Grinstein/Macmillan In one simple hydrolysis step, bacteria make the plasma membrane squishy enough to ease invasion, according to new results from two groups. The groups studied different pathogens, but both came to similar conclusions. Both bacteria, Shigella and Salmonella , inject several invasion-promoting proteins into the host, including a protein with similarity to a mammalian inositol phosphatase. Mauricio Terebiznik, Sergio Grinstein (Hospital for Sick Children, Toronto, ON), and colleagues watched how phosphoinositides were affected during Salmonella infection. They found that one PIP 2 species, PtdIns(4,5)P 2 , was depleted from the base of membrane ruffles that formed where bacteria were pushing to get in, thanks to the phosphatase activity of the SigD effector protein. Like SigD, the Shigella effector IpgD studied by Kirsten Nieburh (Institut Pasteur, Paris, France), Bernard Payrastre (INSERM, Toulouse, France), and colleagues also removed PIP 2 from target cells; in this case, the product was identified as PtdIns(5)P. The result in both cases was a softer plasma membrane. Expression of either phosphatase in mammalian cells caused membrane blebbing and relaxed attachment between the actin cytoskeleton and

Journal

The Journal of Cell BiologyRockefeller University Press

Published: Oct 28, 2002

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