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Sea urchin histamine receptor 1 regulates programmed cell death in larval Strongylocentrotus purpuratus
Settlement is a rapid process in many marine invertebrate species, transitioning a planktonic larva into a benthic juvenile. In indirectly developing sea urchins, this ecological transition correlates with a morphological, developmental and physiological transition (metamorphosis) during which apopt...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5838261/ https://www.ncbi.nlm.nih.gov/pubmed/29507306 http://dx.doi.org/10.1038/s41598-018-22397-4 |
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author | Lutek, Keegan Dhaliwal, Rasmeet Singh Van Raay, Terence J. Heyland, Andreas |
author_facet | Lutek, Keegan Dhaliwal, Rasmeet Singh Van Raay, Terence J. Heyland, Andreas |
author_sort | Lutek, Keegan |
collection | PubMed |
description | Settlement is a rapid process in many marine invertebrate species, transitioning a planktonic larva into a benthic juvenile. In indirectly developing sea urchins, this ecological transition correlates with a morphological, developmental and physiological transition (metamorphosis) during which apoptosis is essential for the resorption and remodelling of larval and juvenile structures. While settlement is initiated by environmental cues (i.e. habitat-specific or benthic substrate cues), metamorphosis is regulated by developmental endocrine signals, such as histamine (HA), thyroid hormones (THs) and nitric oxide (NO). In the purple sea urchin, Strongylocentrotus purpuratus, we found that suH1R mRNA levels increase during larval development and peak during metamorphic competence. SuH1R positive cell clusters are prominently visible in the mouth region of sea urchin larvae, but the protein appears to be expressed at low levels throughout the larval arms and epidermis. SuH1R knock-down experiments in larval stages show that the function of suH1R is in inhibiting apoptosis. Our results therefore suggest that suH1R is regulating the metamorphic transition by inhibiting apoptosis. These results provide new insights into metamorphic mechanisms and have implications for our understanding of settlement and metamorphosis in the marine environment. |
format | Online Article Text |
id | pubmed-5838261 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-58382612018-03-12 Sea urchin histamine receptor 1 regulates programmed cell death in larval Strongylocentrotus purpuratus Lutek, Keegan Dhaliwal, Rasmeet Singh Van Raay, Terence J. Heyland, Andreas Sci Rep Article Settlement is a rapid process in many marine invertebrate species, transitioning a planktonic larva into a benthic juvenile. In indirectly developing sea urchins, this ecological transition correlates with a morphological, developmental and physiological transition (metamorphosis) during which apoptosis is essential for the resorption and remodelling of larval and juvenile structures. While settlement is initiated by environmental cues (i.e. habitat-specific or benthic substrate cues), metamorphosis is regulated by developmental endocrine signals, such as histamine (HA), thyroid hormones (THs) and nitric oxide (NO). In the purple sea urchin, Strongylocentrotus purpuratus, we found that suH1R mRNA levels increase during larval development and peak during metamorphic competence. SuH1R positive cell clusters are prominently visible in the mouth region of sea urchin larvae, but the protein appears to be expressed at low levels throughout the larval arms and epidermis. SuH1R knock-down experiments in larval stages show that the function of suH1R is in inhibiting apoptosis. Our results therefore suggest that suH1R is regulating the metamorphic transition by inhibiting apoptosis. These results provide new insights into metamorphic mechanisms and have implications for our understanding of settlement and metamorphosis in the marine environment. Nature Publishing Group UK 2018-03-05 /pmc/articles/PMC5838261/ /pubmed/29507306 http://dx.doi.org/10.1038/s41598-018-22397-4 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Lutek, Keegan Dhaliwal, Rasmeet Singh Van Raay, Terence J. Heyland, Andreas Sea urchin histamine receptor 1 regulates programmed cell death in larval Strongylocentrotus purpuratus |
title | Sea urchin histamine receptor 1 regulates programmed cell death in larval Strongylocentrotus purpuratus |
title_full | Sea urchin histamine receptor 1 regulates programmed cell death in larval Strongylocentrotus purpuratus |
title_fullStr | Sea urchin histamine receptor 1 regulates programmed cell death in larval Strongylocentrotus purpuratus |
title_full_unstemmed | Sea urchin histamine receptor 1 regulates programmed cell death in larval Strongylocentrotus purpuratus |
title_short | Sea urchin histamine receptor 1 regulates programmed cell death in larval Strongylocentrotus purpuratus |
title_sort | sea urchin histamine receptor 1 regulates programmed cell death in larval strongylocentrotus purpuratus |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5838261/ https://www.ncbi.nlm.nih.gov/pubmed/29507306 http://dx.doi.org/10.1038/s41598-018-22397-4 |
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