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Manipulation of Rho GTPase signaling...

Mohammadi, Sina.

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Manipulation of Rho GTPase signaling during phagocytosis and Yersinia infection.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	Manipulation of Rho GTPase signaling during phagocytosis and Yersinia infection./
Author:	Mohammadi, Sina.
Description:	221 p.
Notes:	Source: Dissertation Abstracts International, Volume: 71-03, Section: B, page: 1486.
Contained By:	Dissertation Abstracts International71-03B.
Subject:	Biology, Cell. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3396567
ISBN:	9781109647686

Manipulation of Rho GTPase signaling during phagocytosis and Yersinia infection.
Mohammadi, Sina.

Manipulation of Rho GTPase signaling during phagocytosis and Yersinia infection. - 221 p.

Source: Dissertation Abstracts International, Volume: 71-03, Section: B, page: 1486.

Thesis (Ph.D.)--Sackler School of Graduate Biomedical Sciences (Tufts University), 2010.

Receptor-mediated phagocytosis, a fundamental process, through which cells internalize extracellular particles, requires the function of Rho family GTPases. We found that the Rho GTPase, Cdc42, functions in a size-dependent manner during phagocytosis. That is, large particle uptake required Cdc42 signaling but small particle uptake did not. This result was consistent with the fact that host cell binding by large particles, but not by small ones, activated Cdc42. Furthermore, a link between Cdc42 signaling and endocytic dynamics during phagocytosis was uncovered. Markers of the endocytic network were found on nascent phagosomes in a size-dependent manner, suggesting that only large particle uptake requires membrane delivery from intracellular pools. Additionally, we found that bulk membrane flow to the cell surface is defective in the absence of Cdc42 signaling and that large particle uptake defect observed in the absence of Cdc42 signaling could be suppressed by increasing membrane flow to the cell surface from the recycling endosome. Taken together, these results describe a new function for Cdc42 during phagocytosis that differs from its previously-characterized role in actin rearrangement.

ISBN: 9781109647686Subjects--Topical Terms:

1017686
Biology, Cell.

Manipulation of Rho GTPase signaling during phagocytosis and Yersinia infection.
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020 $a 9781109647686
035 $a (UMI)AAI3396567
035 $a AAI3396567
040 $a UMI $c UMI
100 1 $a Mohammadi, Sina. $3 1669062
245 1 0 $a Manipulation of Rho GTPase signaling during phagocytosis and Yersinia infection.
300 $a 221 p.
500 $a Source: Dissertation Abstracts International, Volume: 71-03, Section: B, page: 1486.
500 $a Adviser: Ralph R. Isberg.
500 $a Includes supplementary digital materials.
502 $a Thesis (Ph.D.)--Sackler School of Graduate Biomedical Sciences (Tufts University), 2010.
520 $a Receptor-mediated phagocytosis, a fundamental process, through which cells internalize extracellular particles, requires the function of Rho family GTPases. We found that the Rho GTPase, Cdc42, functions in a size-dependent manner during phagocytosis. That is, large particle uptake required Cdc42 signaling but small particle uptake did not. This result was consistent with the fact that host cell binding by large particles, but not by small ones, activated Cdc42. Furthermore, a link between Cdc42 signaling and endocytic dynamics during phagocytosis was uncovered. Markers of the endocytic network were found on nascent phagosomes in a size-dependent manner, suggesting that only large particle uptake requires membrane delivery from intracellular pools. Additionally, we found that bulk membrane flow to the cell surface is defective in the absence of Cdc42 signaling and that large particle uptake defect observed in the absence of Cdc42 signaling could be suppressed by increasing membrane flow to the cell surface from the recycling endosome. Taken together, these results describe a new function for Cdc42 during phagocytosis that differs from its previously-characterized role in actin rearrangement.
520 $a A number of bacterial pathogens such as Yersinia species encode and deliver toxins into the host cell cytosol that misregulate Rho GTPases. Here we show that the Rho GTPase, RhoG, is misregulated by three Y. pseudotuberculosis virulence determinants. Invasin-mediated bacterial binding activates RhoG, while YopE, a translocated Rho GAP, inactivates RhoG. Additionally, the prenylcysteine endoprotease, YopT, cleaves RhoG, thereby mislocalizing it. RhoG is important for proper neutrophil function, so its misregulation may be a way for Y. pseudotuberculosis to avoid immune clearance and thus replicate effectively in the host organism.
590 $a School code: 0845.
650 4 $a Biology, Cell. $3 1017686
650 4 $a Biology, Microbiology. $3 1017734
690 $a 0379
690 $a 0410
710 2 $a Sackler School of Graduate Biomedical Sciences (Tufts University). $b Molecular Microbiology. $3 1669063
773 0 $t Dissertation Abstracts International $g 71-03B.
790 1 0 $a Isberg, Ralph R., $e advisor
790 1 0 $a Mecsas, Joan $e committee member
790 1 0 $a Feig, Larry A. $e committee member
790 1 0 $a Waldor, Matthew K. $e committee member
790 $a 0845
791 $a Ph.D.
792 $a 2010
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3396567