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Impact of the growth anomaly disease...
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Frazier, Monika.
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Impact of the growth anomaly disease on gene expression in the coral, Montipora Capitata, at Wai`opae, Hawai`i.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Impact of the growth anomaly disease on gene expression in the coral, Montipora Capitata, at Wai`opae, Hawai`i./
作者:
Frazier, Monika.
出版者:
Ann Arbor : ProQuest Dissertations & Theses, : 2016,
面頁冊數:
32 p.
附註:
Source: Masters Abstracts International, Volume: 55-04.
Contained By:
Masters Abstracts International55-04(E).
標題:
Molecular biology. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10118988
ISBN:
9781339803050
Impact of the growth anomaly disease on gene expression in the coral, Montipora Capitata, at Wai`opae, Hawai`i.
Frazier, Monika.
Impact of the growth anomaly disease on gene expression in the coral, Montipora Capitata, at Wai`opae, Hawai`i.
- Ann Arbor : ProQuest Dissertations & Theses, 2016 - 32 p.
Source: Masters Abstracts International, Volume: 55-04.
Thesis (M.S.)--University of Hawai'i at Hilo, 2016.
Background Scleractinian corals are a vital component of coral reef ecosystems, which have significant ecological, cultural and economic values worldwide. Anthropogenic and natural stressors are contributing to a global decline in coral health. Assessing coral health is complex due to the presence of a multitude of symbionts that can impact the physiology of the holobiont (coral host and associated symbionts). Growth anomaly (GA) is a coral disease that has significant negative impacts on several biological functions, yet our understanding of its etiology and pathology is lacking. In this study we use high-throughput mRNA sequencing along with de novo transcriptome assembly and ortholog assignment to identify coral genes that are expressed by healthy and GA-affected Montipora capitata coral colonies at a site with high GA prevalence in this species. We conducted pairwise comparisons of three distinct tissue types: healthy tissue from healthy corals, GA lesion tissue from diseased corals ("GA-affected tissue") and apparently healthy tissue from diseased corals ("GA-unaffected tissue").
ISBN: 9781339803050Subjects--Topical Terms:
517296
Molecular biology.
Impact of the growth anomaly disease on gene expression in the coral, Montipora Capitata, at Wai`opae, Hawai`i.
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Background Scleractinian corals are a vital component of coral reef ecosystems, which have significant ecological, cultural and economic values worldwide. Anthropogenic and natural stressors are contributing to a global decline in coral health. Assessing coral health is complex due to the presence of a multitude of symbionts that can impact the physiology of the holobiont (coral host and associated symbionts). Growth anomaly (GA) is a coral disease that has significant negative impacts on several biological functions, yet our understanding of its etiology and pathology is lacking. In this study we use high-throughput mRNA sequencing along with de novo transcriptome assembly and ortholog assignment to identify coral genes that are expressed by healthy and GA-affected Montipora capitata coral colonies at a site with high GA prevalence in this species. We conducted pairwise comparisons of three distinct tissue types: healthy tissue from healthy corals, GA lesion tissue from diseased corals ("GA-affected tissue") and apparently healthy tissue from diseased corals ("GA-unaffected tissue").
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Results The quality-filtered de novo assembled metatranscriptome contained 76,063 genes, of which 13,643 were identified as putative coral genes. A total of 105 coral genes were differentially expressed among tissue types (healthy, GA-affected, GA-unaffected), and included genes involved in immune system pathways, regulation of apoptosis, bone development and growth, as well as disease pathology in other species. Pair-wise comparison of gene expression among healthy, GA-affected and GA-unaffected tissues showed the greatest number of differentially expressed genes between healthy and GA-affected tissues (93 genes), followed by healthy and GA-unaffected tissues (33 genes) and GA-affected and --unaffected tissues (7 genes). Differentially expressed genes of interest include deleted in malignant brain tumors 1, tumor necrosis factor receptor-associated factors 3, 5 and 6, low-density lipoprotein receptor-related proteins 4, 5 and 6, and bone morphogenetic protein 1.
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Conclusion The gene expression data and metatranscriptome assembly developed through this study represent a significant addition to the molecular information available to further our understanding of M. capitata GA. This is the first study to use mRNA-seq to investigate coral GA, and the first RNA-seq metatranscriptome assembly for the M. capitata holobiont. Differentially expressed putative coral genes identified in this study can serve as candidates for future targeted gene expression research in M. capitata GA. Furthermore, in the absence of a sequenced genome for this species of coral, the assembled transcriptome has vast application in the field of coral health.
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