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Peracino, B., Borleis, J., Jin, T., Westphal, M., Schwartz, M., Wu, L., Bracco, E., Gerisch, G., Devreotes, P., Bozzaro, S., (1998) ' G protein beta subunit-null mutants are impaired in phagocytosis and chemotaxis due to inappropriate regulation of the actin cytoskeleton. ' J Cell Biol 141 1529-37

 

Abstract:Chemotaxis and phagocytosis are basically similar in cells of the immune system and in Dictyostelium amebae. Deletion of the unique G protein beta subunit in D. discoideum impaired phagocytosis but had little effect on fluid-phase endocytosis, cytokinesis, or random motility. Constitutive expression of wild-type beta subunit restored phagocytosis and normal development. Chemoattractants released by cells or bacteria trigger typical transient actin polymerization responses in wild-type cells. In beta subunit-null cells, and in a series of beta subunit point mutants, these responses were impaired to a degree that correlated with the defect in phagocytosis. Image analysis of green fluorescent protein-actin transfected cells showed that beta subunit- null cells were defective in reshaping the actin network into a phagocytic cup, and eventually a phagosome, in response to particle attachment. Our results indicate that signaling through heterotrimeric G proteins is required for regulating the actin cytoskeleton during phagocytic uptake, as previously shown for chemotaxis. Inhibitors of phospholipase C and intracellular Ca2+ mobilization inhibited phagocytosis, suggesting the possible involvement of these effectors in the process.
Status:	Published	Type:	Journal article	Source:	PUBMED	PubMed ID:	9647646

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	Genes addressed in this paper
	actin	gpbA
Topics in this paper
Endocytosis		X
Cytoskeleton		X
Regulatory Role		X
Mutants/Phenotypes		X
Growth		X
Function/Process		X
Signal Transduction		X

There are 1 'not yet curated' genes for this paper. actin |