Major Quantitative Trait Loci Affect Resistance to Infectious Pancreatic Necrosis in Atlantic Salmon (Salmo salar)
Infectious pancreatic necrosis (IPN) is a viral disease currently presenting a major problem in the production of Atlantic salmon (Salmon salar). IPN can cause significant mortality to salmon fry within freshwater hatcheries and to smolts following transfer to seawater, although challenged populatio...
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Veröffentlicht in: | Genetics (Austin) 2008-02, Vol.178 (2), p.1109-1115 |
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description | Infectious pancreatic necrosis (IPN) is a viral disease currently presenting a major problem in the production of Atlantic salmon (Salmon salar). IPN can cause significant mortality to salmon fry within freshwater hatcheries and to smolts following transfer to seawater, although challenged populations show clear genetic variation in resistance. To determine whether this genetic variation includes loci of major effect, a genomewide quantitative trait loci (QTL) scan was performed within 10 full-sib families that had received a natural seawater IPN challenge. To utilize the large difference between Atlantic salmon male and female recombination rates, a two-stage mapping strategy was employed. Initially, a sire-based QTL analysis was used to detect linkage groups with significant effects on IPN resistance, using two to three microsatellite markers per linkage group. A dam-based analysis with additional markers was then used to confirm and position any detected QTL. Two genomewide significant QTL and one suggestive QTL were detected in the genome scan. The most significant QTL was mapped to linkage group 21 and was significant at the genomewide level in both the sire and the dam-based analyses. The identified QTL can be applied in marker-assisted selection programs to improve the resistance of salmon to IPN and reduce disease-related mortality. |
doi_str_mv | 10.1534/genetics.107.082974 |
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IPN can cause significant mortality to salmon fry within freshwater hatcheries and to smolts following transfer to seawater, although challenged populations show clear genetic variation in resistance. To determine whether this genetic variation includes loci of major effect, a genomewide quantitative trait loci (QTL) scan was performed within 10 full-sib families that had received a natural seawater IPN challenge. To utilize the large difference between Atlantic salmon male and female recombination rates, a two-stage mapping strategy was employed. Initially, a sire-based QTL analysis was used to detect linkage groups with significant effects on IPN resistance, using two to three microsatellite markers per linkage group. A dam-based analysis with additional markers was then used to confirm and position any detected QTL. Two genomewide significant QTL and one suggestive QTL were detected in the genome scan. The most significant QTL was mapped to linkage group 21 and was significant at the genomewide level in both the sire and the dam-based analyses. The identified QTL can be applied in marker-assisted selection programs to improve the resistance of salmon to IPN and reduce disease-related mortality.</description><identifier>ISSN: 0016-6731</identifier><identifier>ISSN: 1943-2631</identifier><identifier>EISSN: 1943-2631</identifier><identifier>DOI: 10.1534/genetics.107.082974</identifier><identifier>PMID: 18245341</identifier><identifier>CODEN: GENTAE</identifier><language>eng</language><publisher>United States: Genetics Soc America</publisher><subject>Animals ; Aquaculture ; Bacterial Infections - genetics ; Bacterial Infections - pathology ; Bacterial Infections - veterinary ; Chromosome Mapping ; Fish ; Fish Diseases - genetics ; Genomics ; Genotype ; Investigations ; Mortality ; Necrosis ; Pancreatic Diseases - genetics ; Pancreatic Diseases - microbiology ; Pancreatic Diseases - pathology ; Pancreatic Diseases - veterinary ; Quantitative Trait Loci ; Salmo salar - genetics ; Salmon ; Sensitivity and Specificity ; Trout ; United States</subject><ispartof>Genetics (Austin), 2008-02, Vol.178 (2), p.1109-1115</ispartof><rights>Copyright Genetics Society of America Feb 2008</rights><rights>Copyright © 2008 by the Genetics Society of America</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c578t-9f0cd8cb3769c182f9474b24bfd96b135a62903047c9aa72c95fd940481574c23</citedby><cites>FETCH-LOGICAL-c578t-9f0cd8cb3769c182f9474b24bfd96b135a62903047c9aa72c95fd940481574c23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18245341$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Houston, Ross D</creatorcontrib><creatorcontrib>Haley, Chris S</creatorcontrib><creatorcontrib>Hamilton, Alastair</creatorcontrib><creatorcontrib>Guy, Derrick R</creatorcontrib><creatorcontrib>Tinch, Alan E</creatorcontrib><creatorcontrib>Taggart, John B</creatorcontrib><creatorcontrib>McAndrew, Brendan J</creatorcontrib><creatorcontrib>Bishop, Stephen C</creatorcontrib><title>Major Quantitative Trait Loci Affect Resistance to Infectious Pancreatic Necrosis in Atlantic Salmon (Salmo salar)</title><title>Genetics (Austin)</title><addtitle>Genetics</addtitle><description>Infectious pancreatic necrosis (IPN) is a viral disease currently presenting a major problem in the production of Atlantic salmon (Salmon salar). IPN can cause significant mortality to salmon fry within freshwater hatcheries and to smolts following transfer to seawater, although challenged populations show clear genetic variation in resistance. To determine whether this genetic variation includes loci of major effect, a genomewide quantitative trait loci (QTL) scan was performed within 10 full-sib families that had received a natural seawater IPN challenge. To utilize the large difference between Atlantic salmon male and female recombination rates, a two-stage mapping strategy was employed. Initially, a sire-based QTL analysis was used to detect linkage groups with significant effects on IPN resistance, using two to three microsatellite markers per linkage group. A dam-based analysis with additional markers was then used to confirm and position any detected QTL. Two genomewide significant QTL and one suggestive QTL were detected in the genome scan. The most significant QTL was mapped to linkage group 21 and was significant at the genomewide level in both the sire and the dam-based analyses. The identified QTL can be applied in marker-assisted selection programs to improve the resistance of salmon to IPN and reduce disease-related mortality.</description><subject>Animals</subject><subject>Aquaculture</subject><subject>Bacterial Infections - genetics</subject><subject>Bacterial Infections - pathology</subject><subject>Bacterial Infections - veterinary</subject><subject>Chromosome Mapping</subject><subject>Fish</subject><subject>Fish Diseases - genetics</subject><subject>Genomics</subject><subject>Genotype</subject><subject>Investigations</subject><subject>Mortality</subject><subject>Necrosis</subject><subject>Pancreatic Diseases - genetics</subject><subject>Pancreatic Diseases - microbiology</subject><subject>Pancreatic Diseases - pathology</subject><subject>Pancreatic Diseases - veterinary</subject><subject>Quantitative Trait Loci</subject><subject>Salmo salar - genetics</subject><subject>Salmon</subject><subject>Sensitivity and Specificity</subject><subject>Trout</subject><subject>United States</subject><issn>0016-6731</issn><issn>1943-2631</issn><issn>1943-2631</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkVuP0zAQhS0EYsvCL0BCFg9cHlI8thPHL0jVistK5b48W47rtK4Se7Gdrfj3OLRcn0aa-eZ4jg9CD4EsoWb8xdZ6m51JSyBiSVoqBb-FFiA5q2jD4DZaEAJN1QgGZ-heSntCSCPr9i46g5byIgELFN_pfYj406R9dllnd2PxVdQu43UwDq_63pqMP9vkUtbeWJwDvvRz04Up4Y-lF21ZM_i9NTEUDDuPV3mY9Qz-oocxePzsZ8VJDzo-v4_u9HpI9sGpnqOvr19dXbyt1h_eXF6s1pWpRZsr2ROzaU3HRCNNObiXXPCO8q7fyKYDVuuGSsIIF0ZqLaiRdZlwwluoBTeUnaOXR93rqRvtxlifox7UdXSjjt9V0E79O_Fup7bhRlHKW9bUReDJSSCGb5NNWY0uGTsUb7aYV4IwEA3MLz3-D9yHKfpiTlHgwLhoeYHYEZq_KUXb_74EiJoDVb8CLQ2hjoGWrUd_m_izc0qwAE-PwM5tdwcXrUqjHoaCgzocDiBaRRUAkewHMrKsvw</recordid><startdate>20080201</startdate><enddate>20080201</enddate><creator>Houston, Ross D</creator><creator>Haley, Chris S</creator><creator>Hamilton, Alastair</creator><creator>Guy, Derrick R</creator><creator>Tinch, Alan E</creator><creator>Taggart, John B</creator><creator>McAndrew, Brendan J</creator><creator>Bishop, Stephen C</creator><general>Genetics Soc America</general><general>Genetics Society of America</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>4T-</scope><scope>4U-</scope><scope>7QP</scope><scope>7SS</scope><scope>7TK</scope><scope>7TM</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>LK8</scope><scope>M0K</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20080201</creationdate><title>Major Quantitative Trait Loci Affect Resistance to Infectious Pancreatic Necrosis in Atlantic Salmon (Salmo salar)</title><author>Houston, Ross D ; Haley, Chris S ; Hamilton, Alastair ; Guy, Derrick R ; Tinch, Alan E ; Taggart, John B ; McAndrew, Brendan J ; Bishop, Stephen C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c578t-9f0cd8cb3769c182f9474b24bfd96b135a62903047c9aa72c95fd940481574c23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Aquaculture</topic><topic>Bacterial Infections - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genetics (Austin)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Houston, Ross D</au><au>Haley, Chris S</au><au>Hamilton, Alastair</au><au>Guy, Derrick R</au><au>Tinch, Alan E</au><au>Taggart, John B</au><au>McAndrew, Brendan J</au><au>Bishop, Stephen C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Major Quantitative Trait Loci Affect Resistance to Infectious Pancreatic Necrosis in Atlantic Salmon (Salmo salar)</atitle><jtitle>Genetics (Austin)</jtitle><addtitle>Genetics</addtitle><date>2008-02-01</date><risdate>2008</risdate><volume>178</volume><issue>2</issue><spage>1109</spage><epage>1115</epage><pages>1109-1115</pages><issn>0016-6731</issn><issn>1943-2631</issn><eissn>1943-2631</eissn><coden>GENTAE</coden><abstract>Infectious pancreatic necrosis (IPN) is a viral disease currently presenting a major problem in the production of Atlantic salmon (Salmon salar). IPN can cause significant mortality to salmon fry within freshwater hatcheries and to smolts following transfer to seawater, although challenged populations show clear genetic variation in resistance. To determine whether this genetic variation includes loci of major effect, a genomewide quantitative trait loci (QTL) scan was performed within 10 full-sib families that had received a natural seawater IPN challenge. To utilize the large difference between Atlantic salmon male and female recombination rates, a two-stage mapping strategy was employed. Initially, a sire-based QTL analysis was used to detect linkage groups with significant effects on IPN resistance, using two to three microsatellite markers per linkage group. A dam-based analysis with additional markers was then used to confirm and position any detected QTL. Two genomewide significant QTL and one suggestive QTL were detected in the genome scan. The most significant QTL was mapped to linkage group 21 and was significant at the genomewide level in both the sire and the dam-based analyses. The identified QTL can be applied in marker-assisted selection programs to improve the resistance of salmon to IPN and reduce disease-related mortality.</abstract><cop>United States</cop><pub>Genetics Soc America</pub><pmid>18245341</pmid><doi>10.1534/genetics.107.082974</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
subjects | Animals Aquaculture Bacterial Infections - genetics Bacterial Infections - pathology Bacterial Infections - veterinary Chromosome Mapping Fish Fish Diseases - genetics Genomics Genotype Investigations Mortality Necrosis Pancreatic Diseases - genetics Pancreatic Diseases - microbiology Pancreatic Diseases - pathology Pancreatic Diseases - veterinary Quantitative Trait Loci Salmo salar - genetics Salmon Sensitivity and Specificity Trout United States |
title | Major Quantitative Trait Loci Affect Resistance to Infectious Pancreatic Necrosis in Atlantic Salmon (Salmo salar) |
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