A polycystin-type transient receptor potential (Trp) channel that is activated by ATP

ATP and ADP are ancient extra-cellular signalling molecules that in Dictyostelium amoebae cause rapid, transient increases in cytosolic calcium due to an influx through the plasma membrane. This response is independent of hetero-trimeric G-proteins, the putative IP3 receptor IplA and all P2X channel...

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Main Authors: David Traynor, Robert R. Kay
Format: Article
Language:English
Published: The Company of Biologists 2017-02-01
Series:Biology Open
Subjects:
ATP
DIF
Online Access:http://bio.biologists.org/content/6/2/200
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spelling doaj-b1c3ff35ace947db940fd10447ee968d2021-06-02T18:32:39ZengThe Company of BiologistsBiology Open2046-63902017-02-016220020910.1242/bio.020685020685A polycystin-type transient receptor potential (Trp) channel that is activated by ATPDavid Traynor0Robert R. Kay1 MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB1 0QH, UK MRC Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge CB1 0QH, UK ATP and ADP are ancient extra-cellular signalling molecules that in Dictyostelium amoebae cause rapid, transient increases in cytosolic calcium due to an influx through the plasma membrane. This response is independent of hetero-trimeric G-proteins, the putative IP3 receptor IplA and all P2X channels. We show, unexpectedly, that it is abolished in mutants of the polycystin-type transient receptor potential channel, TrpP. Responses to the chemoattractants cyclic-AMP and folic acid are unaffected in TrpP mutants. We report that the DIF morphogens, cyclic-di-GMP, GABA, glutamate and adenosine all induce strong cytoplasmic calcium responses, likewise independently of TrpP. Thus, TrpP is dedicated to purinergic signalling. ATP treatment causes cell blebbing within seconds but this does not require TrpP, implicating a separate purinergic receptor. We could detect no effect of ATP on chemotaxis and TrpP mutants grow, chemotax and develop almost normally in standard conditions. No gating ligand is known for the human homologue of TrpP, polycystin-2, which causes polycystic kidney disease. Our results now show that TrpP mediates purinergic signalling in Dictyostelium and is directly or indirectly gated by ATP.http://bio.biologists.org/content/6/2/200Trp channelPolycystin-2Purinergic signallingATPDIFDictyostelium
collection DOAJ
language English
format Article
sources DOAJ
author David Traynor
Robert R. Kay
spellingShingle David Traynor
Robert R. Kay
A polycystin-type transient receptor potential (Trp) channel that is activated by ATP
Biology Open
Trp channel
Polycystin-2
Purinergic signalling
ATP
DIF
Dictyostelium
author_facet David Traynor
Robert R. Kay
author_sort David Traynor
title A polycystin-type transient receptor potential (Trp) channel that is activated by ATP
title_short A polycystin-type transient receptor potential (Trp) channel that is activated by ATP
title_full A polycystin-type transient receptor potential (Trp) channel that is activated by ATP
title_fullStr A polycystin-type transient receptor potential (Trp) channel that is activated by ATP
title_full_unstemmed A polycystin-type transient receptor potential (Trp) channel that is activated by ATP
title_sort polycystin-type transient receptor potential (trp) channel that is activated by atp
publisher The Company of Biologists
series Biology Open
issn 2046-6390
publishDate 2017-02-01
description ATP and ADP are ancient extra-cellular signalling molecules that in Dictyostelium amoebae cause rapid, transient increases in cytosolic calcium due to an influx through the plasma membrane. This response is independent of hetero-trimeric G-proteins, the putative IP3 receptor IplA and all P2X channels. We show, unexpectedly, that it is abolished in mutants of the polycystin-type transient receptor potential channel, TrpP. Responses to the chemoattractants cyclic-AMP and folic acid are unaffected in TrpP mutants. We report that the DIF morphogens, cyclic-di-GMP, GABA, glutamate and adenosine all induce strong cytoplasmic calcium responses, likewise independently of TrpP. Thus, TrpP is dedicated to purinergic signalling. ATP treatment causes cell blebbing within seconds but this does not require TrpP, implicating a separate purinergic receptor. We could detect no effect of ATP on chemotaxis and TrpP mutants grow, chemotax and develop almost normally in standard conditions. No gating ligand is known for the human homologue of TrpP, polycystin-2, which causes polycystic kidney disease. Our results now show that TrpP mediates purinergic signalling in Dictyostelium and is directly or indirectly gated by ATP.
topic Trp channel
Polycystin-2
Purinergic signalling
ATP
DIF
Dictyostelium
url http://bio.biologists.org/content/6/2/200
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