Loss of Acetylcholine Signaling Reduces Cell Clearance Deficiencies in Caenorhabditis elegans.
The ability to eliminate undesired cells by apoptosis is a key mechanism to maintain organismal health and homeostasis. Failure to clear apoptotic cells efficiently can cause autoimmune diseases in mammals. Genetic studies in Caenorhabditis elegans have greatly helped to decipher the regulation of a...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2016-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC4752328?pdf=render |
| _version_ | 1828270769506877440 |
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| author | Sérgio M Pinto Johann Almendinger Juan Cabello Michael O Hengartner |
| author_facet | Sérgio M Pinto Johann Almendinger Juan Cabello Michael O Hengartner |
| author_sort | Sérgio M Pinto |
| collection | DOAJ |
| description | The ability to eliminate undesired cells by apoptosis is a key mechanism to maintain organismal health and homeostasis. Failure to clear apoptotic cells efficiently can cause autoimmune diseases in mammals. Genetic studies in Caenorhabditis elegans have greatly helped to decipher the regulation of apoptotic cell clearance. In this study, we show that the loss of levamisole-sensitive acetylcholine receptor, but not of a typical neuronal acetylcholine receptor causes a reduction in the number of persistent cell corpses in worms suffering from an engulfment deficiency. This reduction is not caused by impaired or delayed cell death but rather by a partial restoration of the cell clearance capacity. Mutants in acetylcholine turn-over elicit a similar phenotype, implying that acetylcholine signaling is the process responsible for these observations. Surprisingly, tissue specific RNAi suggests that UNC-38, a major component of the levamisole-sensitive receptor, functions in the dying germ cell to influence engulfment efficiency. Animals with loss of acetylcholine receptor exhibit a higher fraction of cell corpses positive for the "eat-me" signal phosphatidylserine. Our results suggest that modulation by ion channels of ion flow across plasma membrane in dying cells can influence the dynamics of phosphatidylserine exposure and thus clearance efficiency. |
| first_indexed | 2024-04-13T05:46:27Z |
| format | Article |
| id | doaj.art-1df654a2ce5e47d3a566d0973467ee98 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-04-13T05:46:27Z |
| publishDate | 2016-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-1df654a2ce5e47d3a566d0973467ee982022-12-22T02:59:56ZengPublic Library of Science (PLoS)PLoS ONE1932-62032016-01-01112e014927410.1371/journal.pone.0149274Loss of Acetylcholine Signaling Reduces Cell Clearance Deficiencies in Caenorhabditis elegans.Sérgio M PintoJohann AlmendingerJuan CabelloMichael O HengartnerThe ability to eliminate undesired cells by apoptosis is a key mechanism to maintain organismal health and homeostasis. Failure to clear apoptotic cells efficiently can cause autoimmune diseases in mammals. Genetic studies in Caenorhabditis elegans have greatly helped to decipher the regulation of apoptotic cell clearance. In this study, we show that the loss of levamisole-sensitive acetylcholine receptor, but not of a typical neuronal acetylcholine receptor causes a reduction in the number of persistent cell corpses in worms suffering from an engulfment deficiency. This reduction is not caused by impaired or delayed cell death but rather by a partial restoration of the cell clearance capacity. Mutants in acetylcholine turn-over elicit a similar phenotype, implying that acetylcholine signaling is the process responsible for these observations. Surprisingly, tissue specific RNAi suggests that UNC-38, a major component of the levamisole-sensitive receptor, functions in the dying germ cell to influence engulfment efficiency. Animals with loss of acetylcholine receptor exhibit a higher fraction of cell corpses positive for the "eat-me" signal phosphatidylserine. Our results suggest that modulation by ion channels of ion flow across plasma membrane in dying cells can influence the dynamics of phosphatidylserine exposure and thus clearance efficiency.http://europepmc.org/articles/PMC4752328?pdf=render |
| spellingShingle | Sérgio M Pinto Johann Almendinger Juan Cabello Michael O Hengartner Loss of Acetylcholine Signaling Reduces Cell Clearance Deficiencies in Caenorhabditis elegans. PLoS ONE |
| title | Loss of Acetylcholine Signaling Reduces Cell Clearance Deficiencies in Caenorhabditis elegans. |
| title_full | Loss of Acetylcholine Signaling Reduces Cell Clearance Deficiencies in Caenorhabditis elegans. |
| title_fullStr | Loss of Acetylcholine Signaling Reduces Cell Clearance Deficiencies in Caenorhabditis elegans. |
| title_full_unstemmed | Loss of Acetylcholine Signaling Reduces Cell Clearance Deficiencies in Caenorhabditis elegans. |
| title_short | Loss of Acetylcholine Signaling Reduces Cell Clearance Deficiencies in Caenorhabditis elegans. |
| title_sort | loss of acetylcholine signaling reduces cell clearance deficiencies in caenorhabditis elegans |
| url | http://europepmc.org/articles/PMC4752328?pdf=render |
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