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De novo metatranscriptome assembly and coral gene expression profile of Montipora capitata with growth anomaly
BACKGROUND: Scleractinian corals are a vital component of coral reef ecosystems, and of significant cultural and economic value worldwide. As anthropogenic and natural stressors are contributing to a global decline of coral reefs, understanding coral health is critical to help preserve these ecosyst...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5594617/ https://www.ncbi.nlm.nih.gov/pubmed/28893194 http://dx.doi.org/10.1186/s12864-017-4090-y |
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author | Frazier, Monika Helmkampf, Martin Bellinger, M. Renee Geib, Scott M. Takabayashi, Misaki |
author_facet | Frazier, Monika Helmkampf, Martin Bellinger, M. Renee Geib, Scott M. Takabayashi, Misaki |
author_sort | Frazier, Monika |
collection | PubMed |
description | BACKGROUND: Scleractinian corals are a vital component of coral reef ecosystems, and of significant cultural and economic value worldwide. As anthropogenic and natural stressors are contributing to a global decline of coral reefs, understanding coral health is critical to help preserve these ecosystems. Growth anomaly (GA) is a coral disease that has significant negative impacts on coral biology, yet our understanding of its etiology and pathology is lacking. In this study we used RNA-seq along with de novo metatranscriptome assembly and homology assignment to identify coral genes that are expressed in three distinct coral tissue types: tissue from healthy corals (“healthy”), GA lesion tissue from diseased corals (“GA-affected”) and apparently healthy tissue from diseased corals (“GA-unaffected”). We conducted pairwise comparisons of gene expression among these three tissue types to identify genes and pathways that help us to unravel the molecular pathology of this coral disease. RESULTS: The quality-filtered de novo-assembled metatranscriptome contained 76,063 genes, of which 13,643 were identified as putative coral genes. Overall gene expression profiles of coral genes revealed high similarity between healthy tissue samples, in contrast to high variance among diseased samples. This indicates GA has a variety of genetic effects at the colony level, including on seemingly healthy (GA-unaffected) tissue. A total of 105 unique coral genes were found differentially expressed among tissue types. Pairwise comparisons revealed the greatest number of differentially expressed genes between healthy and GA-affected tissue (93 genes), followed by healthy and GA-unaffected tissue (33 genes), and GA-affected and -unaffected tissue (7 genes). The putative function of these genes suggests GA is associated with changes in the activity of genes involved in developmental processes and activation of the immune system. CONCLUSION: This is one of the first transcriptome-level studies to investigate coral GA, and the first metatranscriptome assembly for the M. capitata holobiont. The gene expression data, metatranscriptome assembly and methodology developed through this study represent a significant addition to the molecular information available to further our understanding of this coral disease. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12864-017-4090-y) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5594617 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-55946172017-09-15 De novo metatranscriptome assembly and coral gene expression profile of Montipora capitata with growth anomaly Frazier, Monika Helmkampf, Martin Bellinger, M. Renee Geib, Scott M. Takabayashi, Misaki BMC Genomics Research Article BACKGROUND: Scleractinian corals are a vital component of coral reef ecosystems, and of significant cultural and economic value worldwide. As anthropogenic and natural stressors are contributing to a global decline of coral reefs, understanding coral health is critical to help preserve these ecosystems. Growth anomaly (GA) is a coral disease that has significant negative impacts on coral biology, yet our understanding of its etiology and pathology is lacking. In this study we used RNA-seq along with de novo metatranscriptome assembly and homology assignment to identify coral genes that are expressed in three distinct coral tissue types: tissue from healthy corals (“healthy”), GA lesion tissue from diseased corals (“GA-affected”) and apparently healthy tissue from diseased corals (“GA-unaffected”). We conducted pairwise comparisons of gene expression among these three tissue types to identify genes and pathways that help us to unravel the molecular pathology of this coral disease. RESULTS: The quality-filtered de novo-assembled metatranscriptome contained 76,063 genes, of which 13,643 were identified as putative coral genes. Overall gene expression profiles of coral genes revealed high similarity between healthy tissue samples, in contrast to high variance among diseased samples. This indicates GA has a variety of genetic effects at the colony level, including on seemingly healthy (GA-unaffected) tissue. A total of 105 unique coral genes were found differentially expressed among tissue types. Pairwise comparisons revealed the greatest number of differentially expressed genes between healthy and GA-affected tissue (93 genes), followed by healthy and GA-unaffected tissue (33 genes), and GA-affected and -unaffected tissue (7 genes). The putative function of these genes suggests GA is associated with changes in the activity of genes involved in developmental processes and activation of the immune system. CONCLUSION: This is one of the first transcriptome-level studies to investigate coral GA, and the first metatranscriptome assembly for the M. capitata holobiont. The gene expression data, metatranscriptome assembly and methodology developed through this study represent a significant addition to the molecular information available to further our understanding of this coral disease. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s12864-017-4090-y) contains supplementary material, which is available to authorized users. BioMed Central 2017-09-11 /pmc/articles/PMC5594617/ /pubmed/28893194 http://dx.doi.org/10.1186/s12864-017-4090-y Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Frazier, Monika Helmkampf, Martin Bellinger, M. Renee Geib, Scott M. Takabayashi, Misaki De novo metatranscriptome assembly and coral gene expression profile of Montipora capitata with growth anomaly |
title | De novo metatranscriptome assembly and coral gene expression profile of Montipora capitata with growth anomaly |
title_full | De novo metatranscriptome assembly and coral gene expression profile of Montipora capitata with growth anomaly |
title_fullStr | De novo metatranscriptome assembly and coral gene expression profile of Montipora capitata with growth anomaly |
title_full_unstemmed | De novo metatranscriptome assembly and coral gene expression profile of Montipora capitata with growth anomaly |
title_short | De novo metatranscriptome assembly and coral gene expression profile of Montipora capitata with growth anomaly |
title_sort | de novo metatranscriptome assembly and coral gene expression profile of montipora capitata with growth anomaly |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5594617/ https://www.ncbi.nlm.nih.gov/pubmed/28893194 http://dx.doi.org/10.1186/s12864-017-4090-y |
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