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Genetic analysis of the role of G protein–coupled receptor signaling in electrotaxis
Cells display chemotaxis and electrotaxis by migrating directionally in gradients of specific chemicals or electrical potential. Chemotaxis in Dictyostelium discoideum is mediated by G protein–coupled receptors. The unique Gβ is essential for all chemotactic responses, although different chemoattrac...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
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The Rockefeller University Press
2002
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2174050/ https://www.ncbi.nlm.nih.gov/pubmed/12045182 http://dx.doi.org/10.1083/jcb.200112070 |
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author | Zhao, Min Jin, Tian McCaig, Colin D. Forrester, John V. Devreotes, Peter N. |
author_facet | Zhao, Min Jin, Tian McCaig, Colin D. Forrester, John V. Devreotes, Peter N. |
author_sort | Zhao, Min |
collection | PubMed |
description | Cells display chemotaxis and electrotaxis by migrating directionally in gradients of specific chemicals or electrical potential. Chemotaxis in Dictyostelium discoideum is mediated by G protein–coupled receptors. The unique Gβ is essential for all chemotactic responses, although different chemoattractants use different receptors and Gα subunits. Dictyostelium amoebae show striking electrotaxis in an applied direct current electric field. Perhaps electrotaxis and chemotaxis share similar signaling mechanisms? Null mutation of Gβ and cAMP receptor 1 and Gα2 did not abolish electrotaxis, although Gβ-null mutations showed suppressed electrotaxis. By contrast, G protein signaling plays an essential role in chemotaxis. G protein–coupled receptor signaling was monitored with PHcrac–green fluorescent protein, which translocates to inositol phospholipids at the leading edge of cells during chemotaxis. There was no intracellular gradient of this protein during electrotaxis. However, F-actin was polymerized at the leading edge of cells during electrotaxis. We conclude that reception and transduction of the electrotaxis signal are largely independent of G protein–coupled receptor signaling and that the pathways driving chemotaxis and electrotaxis intersect downstream of heterotrimeric G proteins to invoke cytoskeletal elements. |
format | Text |
id | pubmed-2174050 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2002 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-21740502008-05-01 Genetic analysis of the role of G protein–coupled receptor signaling in electrotaxis Zhao, Min Jin, Tian McCaig, Colin D. Forrester, John V. Devreotes, Peter N. J Cell Biol Report Cells display chemotaxis and electrotaxis by migrating directionally in gradients of specific chemicals or electrical potential. Chemotaxis in Dictyostelium discoideum is mediated by G protein–coupled receptors. The unique Gβ is essential for all chemotactic responses, although different chemoattractants use different receptors and Gα subunits. Dictyostelium amoebae show striking electrotaxis in an applied direct current electric field. Perhaps electrotaxis and chemotaxis share similar signaling mechanisms? Null mutation of Gβ and cAMP receptor 1 and Gα2 did not abolish electrotaxis, although Gβ-null mutations showed suppressed electrotaxis. By contrast, G protein signaling plays an essential role in chemotaxis. G protein–coupled receptor signaling was monitored with PHcrac–green fluorescent protein, which translocates to inositol phospholipids at the leading edge of cells during chemotaxis. There was no intracellular gradient of this protein during electrotaxis. However, F-actin was polymerized at the leading edge of cells during electrotaxis. We conclude that reception and transduction of the electrotaxis signal are largely independent of G protein–coupled receptor signaling and that the pathways driving chemotaxis and electrotaxis intersect downstream of heterotrimeric G proteins to invoke cytoskeletal elements. The Rockefeller University Press 2002-06-10 /pmc/articles/PMC2174050/ /pubmed/12045182 http://dx.doi.org/10.1083/jcb.200112070 Text en Copyright © 2002, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Report Zhao, Min Jin, Tian McCaig, Colin D. Forrester, John V. Devreotes, Peter N. Genetic analysis of the role of G protein–coupled receptor signaling in electrotaxis |
title | Genetic analysis of the role of G protein–coupled receptor signaling in electrotaxis |
title_full | Genetic analysis of the role of G protein–coupled receptor signaling in electrotaxis |
title_fullStr | Genetic analysis of the role of G protein–coupled receptor signaling in electrotaxis |
title_full_unstemmed | Genetic analysis of the role of G protein–coupled receptor signaling in electrotaxis |
title_short | Genetic analysis of the role of G protein–coupled receptor signaling in electrotaxis |
title_sort | genetic analysis of the role of g protein–coupled receptor signaling in electrotaxis |
topic | Report |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2174050/ https://www.ncbi.nlm.nih.gov/pubmed/12045182 http://dx.doi.org/10.1083/jcb.200112070 |
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