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Impact of the growth anomaly disease on gene expression in the coral, Montipora Capitata, at Wai`opae, Hawai`i.

Record Type:	Language materials, manuscript : Monograph/item
Title/Author:	Impact of the growth anomaly disease on gene expression in the coral, Montipora Capitata, at Wai`opae, Hawai`i./
Author:	Frazier, Monika.
Description:	1 online resource (32 pages)
Notes:	Source: Masters Abstracts International, Volume: 55-04.
Contained By:	Masters Abstracts International55-04(E).
Subject:	Molecular biology. -
Online resource:	click for full text (PQDT)
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. - 1 online resource (32 pages)

Source: Masters Abstracts International, Volume: 55-04.

Thesis (M.S.)

Includes bibliographical references

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").

Electronic reproduction.
Ann Arbor, Mich. :
ProQuest,
2018

Mode of access: World Wide Web

ISBN: 9781339803050Subjects--Topical Terms:

583443
Molecular biology.
Index Terms--Genre/Form:

554714
Electronic books.

Impact of the growth anomaly disease on gene expression in the coral, Montipora Capitata, at Wai`opae, Hawai`i.
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100 1 $a Frazier, Monika. $3 1178852
245 1 0 $a Impact of the growth anomaly disease on gene expression in the coral, Montipora Capitata, at Wai`opae, Hawai`i.
264 0 $c 2016
300 $a 1 online resource (32 pages)
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500 $a Source: Masters Abstracts International, Volume: 55-04.
500 $a Adviser: Misaki Takabayashi.
502 $a Thesis (M.S.) $c University of Hawai'i at Hilo $d 2016.
504 $a Includes bibliographical references
520 $a 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").
520 $a 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.
520 $a 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.
533 $a Electronic reproduction. $b Ann Arbor, Mich. : $c ProQuest, $d 2018
538 $a Mode of access: World Wide Web
650 4 $a Molecular biology. $3 583443
650 4 $a Genetics. $3 578972
650 4 $a Climate change. $2 bicssc $3 1009004
650 4 $a Ecology. $3 575279
650 4 $a Aquatic sciences. $3 1178821
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710 2 $a University of Hawai'i at Hilo. $b Tropical Conservation Biology and Environmental Science. $3 1178853
773 0 $t Masters Abstracts International $g 55-04(E).
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10118988 $z click for full text (PQDT)