TgrC1 Has Distinct Functions in Dictyostelium Development and Allorecognition

The cell adhesion glycoproteins, TgrB1 and TgrC1, are essential for Dictyostelium development and allorecognition, but it has been impossible to determine whether their pleiotropic roles are due to one common function or to distinct functions in separate pathways. Mutations in the respective genes,...

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Main Authors: Wang, Yue, Shaulsky, Gad
Format: Online
Language:English
Published: Public Library of Science 2015
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404348/
id pubmed-4404348
recordtype oai_dc
spelling pubmed-44043482015-05-02 TgrC1 Has Distinct Functions in Dictyostelium Development and Allorecognition Wang, Yue Shaulsky, Gad Research Article The cell adhesion glycoproteins, TgrB1 and TgrC1, are essential for Dictyostelium development and allorecognition, but it has been impossible to determine whether their pleiotropic roles are due to one common function or to distinct functions in separate pathways. Mutations in the respective genes, tgrB1 and tgrC1, abrogate both development and allorecognition and the defects cannot be suppressed by activation of the cyclic AMP dependent protein kinase PKA, a central regulator of Dictyostelium development. Here we report that mutations in genes outside the known PKA pathway partially suppress the tgrC1-null developmental defect. We separated the pleiotropic roles of tgrC1 by testing the effects of a suppression mutation, stcinsA under different conditions. stcAins modified only the developmental defect of tgrC1– but not the allorecognition defect, suggesting that the two functions are separable. The suppressor mutant phenotype also revealed that tgrC1 regulates stalk differentiation in a cell-autonomous manner and spore differentiation in a non-cell-autonomous manner. Moreover, stcAins did not modify the developmental defect of tgrB1–, but the less robust phenotype of tgrB1– obscures the possible role of stcA relative to tgrB1. Public Library of Science 2015-04-20 /pmc/articles/PMC4404348/ /pubmed/25894230 http://dx.doi.org/10.1371/journal.pone.0124270 Text en © 2015 Wang, Shaulsky http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Wang, Yue
Shaulsky, Gad
spellingShingle Wang, Yue
Shaulsky, Gad
TgrC1 Has Distinct Functions in Dictyostelium Development and Allorecognition
author_facet Wang, Yue
Shaulsky, Gad
author_sort Wang, Yue
title TgrC1 Has Distinct Functions in Dictyostelium Development and Allorecognition
title_short TgrC1 Has Distinct Functions in Dictyostelium Development and Allorecognition
title_full TgrC1 Has Distinct Functions in Dictyostelium Development and Allorecognition
title_fullStr TgrC1 Has Distinct Functions in Dictyostelium Development and Allorecognition
title_full_unstemmed TgrC1 Has Distinct Functions in Dictyostelium Development and Allorecognition
title_sort tgrc1 has distinct functions in dictyostelium development and allorecognition
description The cell adhesion glycoproteins, TgrB1 and TgrC1, are essential for Dictyostelium development and allorecognition, but it has been impossible to determine whether their pleiotropic roles are due to one common function or to distinct functions in separate pathways. Mutations in the respective genes, tgrB1 and tgrC1, abrogate both development and allorecognition and the defects cannot be suppressed by activation of the cyclic AMP dependent protein kinase PKA, a central regulator of Dictyostelium development. Here we report that mutations in genes outside the known PKA pathway partially suppress the tgrC1-null developmental defect. We separated the pleiotropic roles of tgrC1 by testing the effects of a suppression mutation, stcinsA under different conditions. stcAins modified only the developmental defect of tgrC1– but not the allorecognition defect, suggesting that the two functions are separable. The suppressor mutant phenotype also revealed that tgrC1 regulates stalk differentiation in a cell-autonomous manner and spore differentiation in a non-cell-autonomous manner. Moreover, stcAins did not modify the developmental defect of tgrB1–, but the less robust phenotype of tgrB1– obscures the possible role of stcA relative to tgrB1.
publisher Public Library of Science
publishDate 2015
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4404348/
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