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Gene Expression Response to Stony Coral Tissue Loss Disease Transmission in M. cavernosa and O. faveolata From Florida
Since 2014, corals within Florida’s Coral Reef have been dying at an unprecedented rate due to stony coral tissue loss disease (SCTLD). Here we describe the transcriptomic outcomes of three different SCTLD transmission experiments performed at the Smithsonian Marine Station and Mote Marine Laborator...
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Published in: | Frontiers in Marine Science 2021-06, Vol.8 |
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creator | Traylor-Knowles, Nikki Connelly, Michael T. Young, Benjamin D. Eaton, Katherine Muller, Erinn M. Paul, Valerie J. Ushijima, Blake DeMerlis, Allyson Drown, Melissa K. Goncalves, Ashley Kron, Nicholas Snyder, Grace A. Martin, Cecily Rodriguez, Kevin |
description | Since 2014, corals within Florida’s Coral Reef have been dying at an unprecedented rate due to stony coral tissue loss disease (SCTLD). Here we describe the transcriptomic outcomes of three different SCTLD transmission experiments performed at the Smithsonian Marine Station and Mote Marine Laboratory between 2019 and 2020 on the corals
Orbicella faveolata
and
Montastraea cavernosa.
Overall, diseased
O. faveolata
had 2194 differentially expressed genes (DEGs) compared with healthy colonies, whereas diseased
M. cavernosa
had 582 DEGs compared with healthy colonies. Many significant DEGs were implicated in immunity, extracellular matrix rearrangement, and apoptosis. These included, but not limited to, peroxidases, collagens, Bax-like, fibrinogen-like, protein tyrosine kinase, and transforming growth factor beta. A gene module was identified that was significantly correlated to disease transmission. This module possessed many apoptosis and immune genes with high module membership indicating that a complex apoptosis and immune response is occurring in corals during SCTLD transmission. Overall, we found that
O. faveolata
and
M. cavernosa
exhibit an immune, apoptosis, and tissue rearrangement response to SCTLD. We propose that future studies should focus on examining early time points of infection, before the presence of lesions, to understand the activating mechanisms involved in SCTLD. |
doi_str_mv | 10.3389/fmars.2021.681563 |
format | article |
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Orbicella faveolata
and
Montastraea cavernosa.
Overall, diseased
O. faveolata
had 2194 differentially expressed genes (DEGs) compared with healthy colonies, whereas diseased
M. cavernosa
had 582 DEGs compared with healthy colonies. Many significant DEGs were implicated in immunity, extracellular matrix rearrangement, and apoptosis. These included, but not limited to, peroxidases, collagens, Bax-like, fibrinogen-like, protein tyrosine kinase, and transforming growth factor beta. A gene module was identified that was significantly correlated to disease transmission. This module possessed many apoptosis and immune genes with high module membership indicating that a complex apoptosis and immune response is occurring in corals during SCTLD transmission. Overall, we found that
O. faveolata
and
M. cavernosa
exhibit an immune, apoptosis, and tissue rearrangement response to SCTLD. We propose that future studies should focus on examining early time points of infection, before the presence of lesions, to understand the activating mechanisms involved in SCTLD.</description><identifier>ISSN: 2296-7745</identifier><identifier>EISSN: 2296-7745</identifier><identifier>DOI: 10.3389/fmars.2021.681563</identifier><language>eng</language><publisher>Lausanne: Frontiers Research Foundation</publisher><subject>Airports ; Apoptosis ; BAX protein ; Caribbean coral diseases ; Climate change ; Collagen ; Colonies ; Coral reefs ; Corals ; Defence mechanisms ; Disease transmission ; Epidemics ; Experiments ; Extracellular ; Extracellular matrix ; Fibrinogen ; Gene expression ; Growth factors ; Immune response ; Immune system ; Immunity ; Laboratories ; Lesions ; Marine invertebrates ; Pathogens ; Protein-tyrosine kinase ; stony coral tissue loss disease ; Tissue ; transcriptomics ; Transforming growth factor-b ; Tyrosine</subject><ispartof>Frontiers in Marine Science, 2021-06, Vol.8</ispartof><rights>2021. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2973-ae347a8397b3347f134d5dd37ce9ceff722b80fee15c2543870ca13d4312bae13</citedby><cites>FETCH-LOGICAL-c2973-ae347a8397b3347f134d5dd37ce9ceff722b80fee15c2543870ca13d4312bae13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2546392745/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2546392745?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,25753,27924,27925,37012,44590,75126</link.rule.ids></links><search><creatorcontrib>Traylor-Knowles, Nikki</creatorcontrib><creatorcontrib>Connelly, Michael T.</creatorcontrib><creatorcontrib>Young, Benjamin D.</creatorcontrib><creatorcontrib>Eaton, Katherine</creatorcontrib><creatorcontrib>Muller, Erinn M.</creatorcontrib><creatorcontrib>Paul, Valerie J.</creatorcontrib><creatorcontrib>Ushijima, Blake</creatorcontrib><creatorcontrib>DeMerlis, Allyson</creatorcontrib><creatorcontrib>Drown, Melissa K.</creatorcontrib><creatorcontrib>Goncalves, Ashley</creatorcontrib><creatorcontrib>Kron, Nicholas</creatorcontrib><creatorcontrib>Snyder, Grace A.</creatorcontrib><creatorcontrib>Martin, Cecily</creatorcontrib><creatorcontrib>Rodriguez, Kevin</creatorcontrib><title>Gene Expression Response to Stony Coral Tissue Loss Disease Transmission in M. cavernosa and O. faveolata From Florida</title><title>Frontiers in Marine Science</title><description>Since 2014, corals within Florida’s Coral Reef have been dying at an unprecedented rate due to stony coral tissue loss disease (SCTLD). Here we describe the transcriptomic outcomes of three different SCTLD transmission experiments performed at the Smithsonian Marine Station and Mote Marine Laboratory between 2019 and 2020 on the corals
Orbicella faveolata
and
Montastraea cavernosa.
Overall, diseased
O. faveolata
had 2194 differentially expressed genes (DEGs) compared with healthy colonies, whereas diseased
M. cavernosa
had 582 DEGs compared with healthy colonies. Many significant DEGs were implicated in immunity, extracellular matrix rearrangement, and apoptosis. These included, but not limited to, peroxidases, collagens, Bax-like, fibrinogen-like, protein tyrosine kinase, and transforming growth factor beta. A gene module was identified that was significantly correlated to disease transmission. This module possessed many apoptosis and immune genes with high module membership indicating that a complex apoptosis and immune response is occurring in corals during SCTLD transmission. Overall, we found that
O. faveolata
and
M. cavernosa
exhibit an immune, apoptosis, and tissue rearrangement response to SCTLD. We propose that future studies should focus on examining early time points of infection, before the presence of lesions, to understand the activating mechanisms involved in SCTLD.</description><subject>Airports</subject><subject>Apoptosis</subject><subject>BAX protein</subject><subject>Caribbean coral diseases</subject><subject>Climate change</subject><subject>Collagen</subject><subject>Colonies</subject><subject>Coral reefs</subject><subject>Corals</subject><subject>Defence mechanisms</subject><subject>Disease transmission</subject><subject>Epidemics</subject><subject>Experiments</subject><subject>Extracellular</subject><subject>Extracellular matrix</subject><subject>Fibrinogen</subject><subject>Gene expression</subject><subject>Growth factors</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunity</subject><subject>Laboratories</subject><subject>Lesions</subject><subject>Marine invertebrates</subject><subject>Pathogens</subject><subject>Protein-tyrosine kinase</subject><subject>stony coral tissue loss disease</subject><subject>Tissue</subject><subject>transcriptomics</subject><subject>Transforming growth factor-b</subject><subject>Tyrosine</subject><issn>2296-7745</issn><issn>2296-7745</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpNUV1rGzEQPEoDNUl-QN8EffZV0t6XHotrpwGHQOs8i7W0KjJnyZXOIfn3lXMl9GmHZXZmmamqz4LXAIP66o6Yci25FHU3iLaDD9VCStUt-75pP_6HP1W3OR845wIa3jZqUT3fUSC2fjklytnHwH5SPsWQiU2R_ZpieGWrmHBkO5_zmdg25sy--0xYKLuEIR_9fOgDe6iZwWdKIWZkGCx7rJkrizjihGyT4pFtxpi8xZvqyuGY6fbfvK6eNuvd6sdy-3h3v_q2XRqpelgiQdPjAKrfQ0GuvG1ba6E3pAw510u5H7gjEq2RbQNDzw0KsA0IuUcScF3dz7o24kGfki9JveqIXr8tYvqtMU3ejKTlwLtWub0CaZuu-FtpzQWXhIUjKFpfZq1Tin_OlCd9iOcUyvu6eHegZEm4sMTMMqlElci9uwquL23pt7b0pS09twV_AdckiEQ</recordid><startdate>20210629</startdate><enddate>20210629</enddate><creator>Traylor-Knowles, Nikki</creator><creator>Connelly, Michael T.</creator><creator>Young, Benjamin D.</creator><creator>Eaton, Katherine</creator><creator>Muller, Erinn M.</creator><creator>Paul, Valerie J.</creator><creator>Ushijima, Blake</creator><creator>DeMerlis, Allyson</creator><creator>Drown, Melissa K.</creator><creator>Goncalves, Ashley</creator><creator>Kron, Nicholas</creator><creator>Snyder, Grace A.</creator><creator>Martin, Cecily</creator><creator>Rodriguez, Kevin</creator><general>Frontiers Research Foundation</general><general>Frontiers Media S.A</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TN</scope><scope>7XB</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>F1W</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2P</scope><scope>M7P</scope><scope>PCBAR</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>DOA</scope></search><sort><creationdate>20210629</creationdate><title>Gene Expression Response to Stony Coral Tissue Loss Disease Transmission in M. cavernosa and O. faveolata From Florida</title><author>Traylor-Knowles, Nikki ; Connelly, Michael T. ; Young, Benjamin D. ; Eaton, Katherine ; Muller, Erinn M. ; Paul, Valerie J. ; Ushijima, Blake ; DeMerlis, Allyson ; Drown, Melissa K. ; Goncalves, Ashley ; Kron, Nicholas ; Snyder, Grace A. ; Martin, Cecily ; Rodriguez, Kevin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2973-ae347a8397b3347f134d5dd37ce9ceff722b80fee15c2543870ca13d4312bae13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Airports</topic><topic>Apoptosis</topic><topic>BAX protein</topic><topic>Caribbean coral diseases</topic><topic>Climate change</topic><topic>Collagen</topic><topic>Colonies</topic><topic>Coral reefs</topic><topic>Corals</topic><topic>Defence mechanisms</topic><topic>Disease transmission</topic><topic>Epidemics</topic><topic>Experiments</topic><topic>Extracellular</topic><topic>Extracellular matrix</topic><topic>Fibrinogen</topic><topic>Gene expression</topic><topic>Growth factors</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunity</topic><topic>Laboratories</topic><topic>Lesions</topic><topic>Marine invertebrates</topic><topic>Pathogens</topic><topic>Protein-tyrosine kinase</topic><topic>stony coral tissue loss disease</topic><topic>Tissue</topic><topic>transcriptomics</topic><topic>Transforming growth factor-b</topic><topic>Tyrosine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Traylor-Knowles, Nikki</creatorcontrib><creatorcontrib>Connelly, Michael T.</creatorcontrib><creatorcontrib>Young, Benjamin D.</creatorcontrib><creatorcontrib>Eaton, Katherine</creatorcontrib><creatorcontrib>Muller, Erinn M.</creatorcontrib><creatorcontrib>Paul, Valerie J.</creatorcontrib><creatorcontrib>Ushijima, Blake</creatorcontrib><creatorcontrib>DeMerlis, Allyson</creatorcontrib><creatorcontrib>Drown, Melissa K.</creatorcontrib><creatorcontrib>Goncalves, Ashley</creatorcontrib><creatorcontrib>Kron, Nicholas</creatorcontrib><creatorcontrib>Snyder, Grace A.</creatorcontrib><creatorcontrib>Martin, Cecily</creatorcontrib><creatorcontrib>Rodriguez, Kevin</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Oceanic Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Earth, Atmospheric & Aquatic Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>Biological Sciences</collection><collection>ProQuest Science Journals</collection><collection>Biological Science Database</collection><collection>Earth, Atmospheric & Aquatic Science Database</collection><collection>ProQuest Publicly Available Content database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Directory of Open Access Journals at publisher websites</collection><jtitle>Frontiers in Marine Science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Traylor-Knowles, Nikki</au><au>Connelly, Michael T.</au><au>Young, Benjamin D.</au><au>Eaton, Katherine</au><au>Muller, Erinn M.</au><au>Paul, Valerie J.</au><au>Ushijima, Blake</au><au>DeMerlis, Allyson</au><au>Drown, Melissa K.</au><au>Goncalves, Ashley</au><au>Kron, Nicholas</au><au>Snyder, Grace A.</au><au>Martin, Cecily</au><au>Rodriguez, Kevin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gene Expression Response to Stony Coral Tissue Loss Disease Transmission in M. cavernosa and O. faveolata From Florida</atitle><jtitle>Frontiers in Marine Science</jtitle><date>2021-06-29</date><risdate>2021</risdate><volume>8</volume><issn>2296-7745</issn><eissn>2296-7745</eissn><abstract>Since 2014, corals within Florida’s Coral Reef have been dying at an unprecedented rate due to stony coral tissue loss disease (SCTLD). Here we describe the transcriptomic outcomes of three different SCTLD transmission experiments performed at the Smithsonian Marine Station and Mote Marine Laboratory between 2019 and 2020 on the corals
Orbicella faveolata
and
Montastraea cavernosa.
Overall, diseased
O. faveolata
had 2194 differentially expressed genes (DEGs) compared with healthy colonies, whereas diseased
M. cavernosa
had 582 DEGs compared with healthy colonies. Many significant DEGs were implicated in immunity, extracellular matrix rearrangement, and apoptosis. These included, but not limited to, peroxidases, collagens, Bax-like, fibrinogen-like, protein tyrosine kinase, and transforming growth factor beta. A gene module was identified that was significantly correlated to disease transmission. This module possessed many apoptosis and immune genes with high module membership indicating that a complex apoptosis and immune response is occurring in corals during SCTLD transmission. Overall, we found that
O. faveolata
and
M. cavernosa
exhibit an immune, apoptosis, and tissue rearrangement response to SCTLD. We propose that future studies should focus on examining early time points of infection, before the presence of lesions, to understand the activating mechanisms involved in SCTLD.</abstract><cop>Lausanne</cop><pub>Frontiers Research Foundation</pub><doi>10.3389/fmars.2021.681563</doi><oa>free_for_read</oa></addata></record> |
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subjects | Airports Apoptosis BAX protein Caribbean coral diseases Climate change Collagen Colonies Coral reefs Corals Defence mechanisms Disease transmission Epidemics Experiments Extracellular Extracellular matrix Fibrinogen Gene expression Growth factors Immune response Immune system Immunity Laboratories Lesions Marine invertebrates Pathogens Protein-tyrosine kinase stony coral tissue loss disease Tissue transcriptomics Transforming growth factor-b Tyrosine |
title | Gene Expression Response to Stony Coral Tissue Loss Disease Transmission in M. cavernosa and O. faveolata From Florida |
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