Whole-genome sequencing identifies interferon-induced protein IFI6/IFI27-like as a strong candidate gene for VNN resistance in European sea bass.
Journal
Genetics, selection, evolution : GSE
ISSN: 1297-9686
Titre abrégé: Genet Sel Evol
Pays: France
ID NLM: 9114088
Informations de publication
Date de publication:
04 May 2023
04 May 2023
Historique:
received:
28
06
2022
accepted:
18
04
2023
medline:
8
5
2023
pubmed:
5
5
2023
entrez:
4
5
2023
Statut:
epublish
Résumé
Viral nervous necrosis (VNN) is a major disease that affects European sea bass, and understanding the biological mechanisms that underlie VNN resistance is important for the welfare of farmed fish and sustainability of production systems. The aim of this study was to identify genomic regions and genes that are associated with VNN resistance in sea bass. We generated a dataset of 838,451 single nucleotide polymorphisms (SNPs) identified from whole-genome sequencing (WGS) in the parental generation of two commercial populations (A: 2371 individuals and B: 3428 individuals) of European sea bass with phenotypic records for binary survival in a VNN challenge. For each population, three cohorts were submitted to a red-spotted grouper nervous necrosis virus (RGNNV) challenge by immersion and genotyped on a 57K SNP chip. After imputation of WGS SNPs from their parents, quantitative trait loci (QTL) were mapped using a Bayesian sparse linear mixed model (BSLMM). We found several QTL regions that were specific to one of the populations on different linkage groups (LG), and one 127-kb QTL region on LG12 that was shared by both populations and included the genes ZDHHC14, which encodes a palmitoyltransferase, and IFI6/IFI27-like, which encodes an interferon-alpha induced protein. The most significant SNP in this QTL region was only 1.9 kb downstream of the coding sequence of the IFI6/IFI27-like gene. An unrelated population of four large families was used to validate the effect of the QTL. Survival rates of susceptible genotypes were 40.6% and 45.4% in populations A and B, respectively, while that of the resistant genotype was 66.2% in population B and 78% in population A. We have identified a genomic region that carries a major QTL for resistance to VNN and includes the ZDHHC14 and IFI6/IFI27-like genes. The potential involvement of the interferon pathway, a well-known anti-viral defense mechanism in several organisms (chicken, human, or fish), in survival to VNN infection is of particular interest. Our results can lead to major improvements for sea bass breeding programs through marker-assisted genomic selection to obtain more resistant fish.
Sections du résumé
BACKGROUND
BACKGROUND
Viral nervous necrosis (VNN) is a major disease that affects European sea bass, and understanding the biological mechanisms that underlie VNN resistance is important for the welfare of farmed fish and sustainability of production systems. The aim of this study was to identify genomic regions and genes that are associated with VNN resistance in sea bass.
RESULTS
RESULTS
We generated a dataset of 838,451 single nucleotide polymorphisms (SNPs) identified from whole-genome sequencing (WGS) in the parental generation of two commercial populations (A: 2371 individuals and B: 3428 individuals) of European sea bass with phenotypic records for binary survival in a VNN challenge. For each population, three cohorts were submitted to a red-spotted grouper nervous necrosis virus (RGNNV) challenge by immersion and genotyped on a 57K SNP chip. After imputation of WGS SNPs from their parents, quantitative trait loci (QTL) were mapped using a Bayesian sparse linear mixed model (BSLMM). We found several QTL regions that were specific to one of the populations on different linkage groups (LG), and one 127-kb QTL region on LG12 that was shared by both populations and included the genes ZDHHC14, which encodes a palmitoyltransferase, and IFI6/IFI27-like, which encodes an interferon-alpha induced protein. The most significant SNP in this QTL region was only 1.9 kb downstream of the coding sequence of the IFI6/IFI27-like gene. An unrelated population of four large families was used to validate the effect of the QTL. Survival rates of susceptible genotypes were 40.6% and 45.4% in populations A and B, respectively, while that of the resistant genotype was 66.2% in population B and 78% in population A.
CONCLUSIONS
CONCLUSIONS
We have identified a genomic region that carries a major QTL for resistance to VNN and includes the ZDHHC14 and IFI6/IFI27-like genes. The potential involvement of the interferon pathway, a well-known anti-viral defense mechanism in several organisms (chicken, human, or fish), in survival to VNN infection is of particular interest. Our results can lead to major improvements for sea bass breeding programs through marker-assisted genomic selection to obtain more resistant fish.
Identifiants
pubmed: 37143017
doi: 10.1186/s12711-023-00805-2
pii: 10.1186/s12711-023-00805-2
pmc: PMC10161657
doi:
Substances chimiques
Interferons
9008-11-1
IFI6 protein, human
0
Mitochondrial Proteins
0
IFI27 protein, human
0
Membrane Proteins
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
30Subventions
Organisme : FEAMP
ID : FEA470016FA1000005
Organisme : FEAMP
ID : FEA470020FA1000002
Informations de copyright
© 2023. The Author(s).
Références
Nature. 2011 Apr 28;472(7344):481-5
pubmed: 21478870
Dev Comp Immunol. 2014 Oct;46(2):117-28
pubmed: 24731841
J Anim Sci. 2004;82 E-Suppl:E313-328
pubmed: 15471812
Dis Aquat Organ. 2001 Oct 29;47(1):33-8
pubmed: 11797913
Genet Sel Evol. 2021 Apr 1;53(1):32
pubmed: 33794770
Gigascience. 2015 Feb 25;4:7
pubmed: 25722852
Fish Shellfish Immunol. 2016 Jun;53:35-49
pubmed: 26997200
Front Genet. 2022 Mar 25;13:804584
pubmed: 35401661
Fish Shellfish Immunol Rep. 2022 Mar 08;3:100054
pubmed: 36419602
Dis Aquat Organ. 2016 May 26;119(3):231-8
pubmed: 27225206
Am J Hum Genet. 2007 Sep;81(3):559-75
pubmed: 17701901
Nat Genet. 2014 Aug;46(8):858-65
pubmed: 25017103
Mar Biotechnol (NY). 2017 Jun;19(3):255-265
pubmed: 28484864
Bioinformatics. 2009 Jul 15;25(14):1754-60
pubmed: 19451168
Cell. 2018 Jan 25;172(3):423-438.e25
pubmed: 29249360
Front Immunol. 2021 Apr 01;12:634937
pubmed: 33868257
BMC Genet. 2016 Jun 21;17(1):88
pubmed: 27328805
PLoS Genet. 2013;9(2):e1003264
pubmed: 23408905
Immunol Lett. 2012 Nov-Dec;148(1):23-33
pubmed: 22902399
Nat Rev Genet. 2009 Oct;10(10):681-90
pubmed: 19763151
Mol Genet Genomics. 2017 Feb;292(1):231-242
pubmed: 27826737
Cell Microbiol. 2020 Sep;22(9):e13216
pubmed: 32388899
Nat Commun. 2014 Dec 23;5:5770
pubmed: 25534655
Bioinformatics. 2021 Apr 5;36(24):5582-5589
pubmed: 33399819
Gigascience. 2021 Feb 16;10(2):
pubmed: 33590861
Fish Shellfish Immunol. 2014 Oct;40(2):441-5
pubmed: 25107694
Vet Res. 2020 May 12;51(1):64
pubmed: 32398117
Vet Res. 2016 Jan 08;47:6
pubmed: 26743933
Fly (Austin). 2012 Apr-Jun;6(2):80-92
pubmed: 22728672
J Biol Chem. 2017 Dec 29;292(52):21517-21526
pubmed: 29079573
Vaccine. 2011 Mar 24;29(15):2657-71
pubmed: 21320546
Front Genet. 2021 Jul 14;12:665920
pubmed: 34335683
Fish Shellfish Immunol. 2015 Feb;42(2):345-52
pubmed: 25463297
J Fish Dis. 2017 May;40(5):717-742
pubmed: 27633881
BMC Genomics. 2004 Jan 19;5(1):8
pubmed: 14728724
Fish Shellfish Immunol. 2019 Feb;85:78-84
pubmed: 29175472
Fish Shellfish Immunol. 2019 May;88:458-463
pubmed: 30877059
BMC Genomics. 2014 Jun 17;15:478
pubmed: 24935670
Mol Ecol Resour. 2020 Mar;20(2):579-590
pubmed: 31609085
Genet Sel Evol. 2018 Jun 8;50(1):30
pubmed: 29884113
Nat Rev Genet. 2002 Jan;3(1):22-32
pubmed: 11823788
Proc Natl Acad Sci U S A. 2017 Feb 21;114(8):2018-2023
pubmed: 28159892