scholarly journals Investigating mechanisms underlying genetic resistance to Salmon Rickettsial Syndrome in Atlantic salmon using RNA sequencing

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Carolina P. Moraleda ◽  
Diego Robledo ◽  
Alejandro P. Gutiérrez ◽  
Jorge del-Pozo ◽  
José M. Yáñez ◽  
...  
Keyword(s):  
Atlantic Salmon ◽  
Rna Sequencing ◽  
Host Resistance ◽  
Large Population ◽  
Genetic Resistance ◽  
Head Kidney ◽  
Breeding Values ◽  
Association Analyses ◽  
Polygenic Trait ◽  
Salmon Rickettsial Syndrome

Abstract Background Salmon Rickettsial Syndrome (SRS), caused by Piscirickettsia salmonis, is one of the primary causes of morbidity and mortality in Atlantic salmon aquaculture, particularly in Chile. Host resistance is a heritable trait, and functional genomic studies have highlighted genes and pathways important in the response of salmon to the bacteria. However, the functional mechanisms underpinning genetic resistance are not yet well understood. In the current study, a large population of salmon pre-smolts were challenged with P. salmonis, with mortality levels recorded and samples taken for genotyping. In parallel, head kidney and liver samples were taken from animals of the same population with high and low genomic breeding values for resistance, and used for RNA-Sequencing to compare their transcriptome profile both pre and post infection. Results A significant and moderate heritability (h2 = 0.43) was shown for the trait of binary survival. Genome-wide association analyses using 38 K imputed SNP genotypes across 2265 animals highlighted that resistance is a polygenic trait. Several thousand genes were identified as differentially expressed between controls and infected samples, and enriched pathways related to the host immune response were highlighted. In addition, several networks with significant correlation with SRS resistance breeding values were identified, suggesting their involvement in mediating genetic resistance. These included apoptosis, cytoskeletal organisation, and the inflammasome. Conclusions While resistance to SRS is a polygenic trait, this study has highlighted several relevant networks and genes that are likely to play a role in mediating genetic resistance. These genes may be future targets for functional studies, including genome editing, to further elucidate their role underpinning genetic variation in host resistance.

scholarly journals Investigating mechanisms underlying genetic resistance to Salmon Rickettsial Syndrome in Atlantic salmon using RNA sequencing

2020 ◽  
Author(s):  
Carolina P. Moraleda ◽  
Diego Robledo ◽  
Alejandro P. Gutiérrez ◽  
Jorge del-Pozo ◽  
José M. Yáñez ◽  
...  
Keyword(s):  
Atlantic Salmon ◽  
Rna Sequencing ◽  
Host Resistance ◽  
Large Population ◽  
Genetic Resistance ◽  
Head Kidney ◽  
Breeding Values ◽  
Association Analyses ◽  
Polygenic Trait ◽  
Salmon Rickettsial Syndrome

ABSTRACTBackgroundSalmon Rickettsial Syndrome (SRS), caused by Piscirickettsia salmonis, is one of the primary causes of morbidity and mortality in Atlantic salmon aquaculture, particularly in Chile. Host resistance is a heritable trait, and functional genomic studies have highlighted genes and pathways important in the response of salmon to the bacteria. However, the functional mechanisms underpinning genetic resistance are not yet well understood. In the current study, a large population of salmon pre-smolts were challenged with P. salmonis, with mortality levels recorded and samples taken for genotyping. In parallel, head kidney and liver samples were taken from animals of the same population with high and low genomic breeding values for resistance, and used for RNA-Sequencing to compare their transcriptome profile both pre and post infection.ResultsA significant and moderate heritability (h2 = 0.43) was shown for the trait of binary survival. Genome-wide association analyses using 38K imputed SNP genotypes across 2,251 animals highlighted that resistance is a polygenic trait. Several thousand genes were identified as differentially expressed between controls and infected samples, and enriched pathways related to the host immune response were highlighted. In addition, several networks with significant correlation with SRS resistance breeding values were identified, suggesting their involvement in mediating genetic resistance. These included apoptosis, cytoskeletal organisation, and the inflammasome.ConclusionsWhile resistance to SRS is a polygenic trait, this study has highlighted several relevant networks and genes that are likely to play a role in mediating genetic resistance. These genes may be future targets for functional studies, including genome editing, to further elucidate their role underpinning genetic variation in host resistance.

scholarly journals Characterising the mechanisms underlying genetic resistance to amoebic gill disease in Atlantic salmon using RNA sequencing

BMC Genomics ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Diego Robledo ◽  
Alastair Hamilton ◽  
Alejandro P. Gutiérrez ◽  
James E. Bron ◽  
Ross D. Houston
Keyword(s):  
Atlantic Salmon ◽  
Rna Sequencing ◽  
Genetic Resistance ◽  
Gill Disease

scholarly journals Exploring genetic resistance to infectious salmon anaemia virus in Atlantic salmon by genome-wide association and RNA sequencing

BMC Genomics ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
O. Gervais ◽  
A. Barria ◽  
A. Papadopoulou ◽  
R. L. Gratacap ◽  
B. Hillestad ◽  
...  
Keyword(s):  
Atlantic Salmon ◽  
Rna Sequencing ◽  
Post Infection ◽  
Genome Wide Association ◽  
Control Fish ◽  
Infectious Salmon Anaemia Virus ◽  
Transcriptomic Response ◽  
Breeding Values ◽  
Genome Wide ◽  
Interferon Pathway

Abstract Background Infectious Salmonid Anaemia Virus (ISAV) causes a notifiable disease that poses a large threat for Atlantic salmon (Salmo salar) aquaculture worldwide. There is no fully effective treatment or vaccine, and therefore selective breeding to increase resistance to ISAV is a promising avenue for disease prevention. Genomic selection and potentially genome editing can be applied to enhance host resistance, and these approaches benefit from improved knowledge of the genetic and functional basis of the target trait. The aim of this study was to characterise the genetic architecture of resistance to ISAV in a commercial Atlantic salmon population and study its underlying functional genomic basis using RNA Sequencing. Results A total of 2833 Atlantic salmon parr belonging to 194 families were exposed to ISAV in a cohabitation challenge in which cumulative mortality reached 63% over 55 days. A total of 1353 animals were genotyped using a 55 K SNP array, and the estimate of heritability for the trait of binary survival was 0.13–0.33 (pedigree-genomic). A genome-wide association analysis confirmed that resistance to ISAV was a polygenic trait, albeit a genomic region in chromosome Ssa13 was significantly associated with resistance and explained 3% of the genetic variance. RNA sequencing of the heart of 16 infected (7 and 14 days post infection) and 8 control fish highlighted 4927 and 2437 differentially expressed genes at 7 and 14 days post infection respectively. The complement and coagulation pathway was down-regulated in infected fish, while several metabolic pathways were up-regulated. The interferon pathway showed little evidence of up-regulation at 7 days post infection but was mildly activated at 14 days, suggesting a potential crosstalk between host and virus. Comparison of the transcriptomic response of fish with high and low breeding values for resistance highlighted TRIM25 as being up-regulated in resistant fish. Conclusions ISAV resistance shows moderate heritability with a polygenic architecture, but a significant QTL was detected on chromosome 13. A mild up-regulation of the interferon pathway characterises the response to the virus in heart samples from this population of Atlantic salmon, and candidate genes showing differential expression between samples with high and low breeding values for resistance were identified.

scholarly journals Characterising the mechanisms underlying genetic resistance to amoebic gill disease in Atlantic salmon using RNA sequencing

2019 ◽  
Author(s):  
Diego Robledo ◽  
Alastair Hamilton ◽  
Alejandro P. Gutiérrez ◽  
James E. Bron ◽  
Ross D. Houston
Keyword(s):  
Atlantic Salmon ◽  
Differential Expression ◽  
Candidate Genes ◽  
Control Strategies ◽  
Genetic Resistance ◽  
Head Kidney ◽  
Chromosome 17 ◽  
Specific Expression ◽  
Functional Studies ◽  
Gill Disease

ABSTRACTBackgroundGill health is one of the main concerns for Atlantic salmon aquaculture, and Amoebic Gill Disease (AGD), attributable to infection by the amoeba Neoparamoeba perurans, is a frequent cause of morbidity. In the absence of preventive measures, increasing genetic resistance of salmon to AGD via selective breeding can reduce the incidence of the disease and mitigate gill damage. Understanding the mechanisms leading to AGD resistance and the underlying causative genomic features can aid in this effort, while also providing critical information for the development of other control strategies. AGD resistance is considered to be moderately heritable, and several putative QTL have been identified. The aim of the current study was to improve understanding of the mechanisms underlying AGD resistance, and to identify putative causative genomic factors underlying the QTL. To achieve this, RNA was extracted from the gill and head kidney of AGD resistant and susceptible animals following a challenge with N. perurans, and sequenced.ResultsComparison between resistant and susceptible animals pointed to differences mainly in the local immune response in the gill, involving red blood cell genes and genes related to immune function and cell adhesion. Differentially expressed immune genes highlighted differences in the Th2 and Th17 responses, which are consistent with the increased heritability observed after successive challenges with the amoeba. Five QTL-region candidate genes showed differential expression, including a gene connected to interferon responses (GVINP1), a gene involved in systemic inflammation (MAP4K4), and a positive regulator of apoptosis (TRIM39). Analyses of allele-specific expression highlighted a gene in the QTL region on chromosome 17, cellular repressor of E1A-stimulated genes 1 (CREG1), showing allelic differential expression suggestive of a cis-acting regulatory variant.ConclusionsIn summary, this study provides new insights into the mechanisms of resistance to AGD in Atlantic salmon, and highlights candidate genes for further functional studies that can further elucidate the genomic mechanisms leading to resistance and contribute to enhancing salmon health via improved genomic selection.

scholarly journals Differential response of digesta- and mucosa-associated intestinal microbiota to dietary insect meal during the seawater phase of Atlantic salmon

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Yanxian Li ◽  
Leonardo Bruni ◽  
Alexander Jaramillo-Torres ◽  
Karina Gajardo ◽  
Trond M. Kortner ◽  
...  
Keyword(s):  
Atlantic Salmon ◽  
Immune Responses ◽  
Intestinal Microbiota ◽  
Barrier Function ◽  
16S Rrna Gene Sequencing ◽  
Rrna Gene ◽  
Association Analyses ◽  
Distal Intestine ◽  
Expression Of Genes ◽  
Rrna Gene Sequencing

Abstract Background Intestinal digesta is commonly used for studying responses of microbiota to dietary shifts, yet evidence is accumulating that it represents an incomplete view of the intestinal microbiota. The present work aims to investigate the differences between digesta- and mucosa-associated intestinal microbiota in Atlantic salmon (Salmo salar) and how they may respond differently to dietary perturbations. In a 16-week seawater feeding trial, Atlantic salmon were fed either a commercially-relevant reference diet or an insect meal diet containing ~ 15% black soldier fly (Hermetia illucens) larvae meal. The digesta- and mucosa-associated distal intestinal microbiota were profiled by 16S rRNA gene sequencing. Results Regardless of diet, we observed substantial differences between digesta- and mucosa-associated intestinal microbiota. Microbial richness and diversity were much higher in the digesta than the mucosa. The insect meal diet altered the distal intestinal microbiota resulting in higher microbial richness and diversity. The diet effect, however, depended on the sample origin. Digesta-associated intestinal microbiota showed more pronounced changes than the mucosa-associated microbiota. Multivariate association analyses identified two mucosa-enriched taxa, Brevinema andersonii and Spirochaetaceae, associated with the expression of genes related to immune responses and barrier function in the distal intestine, respectively. Conclusions Our data show that salmon intestinal digesta and mucosa harbor microbial communities with clear differences. While feeding insects increased microbial richness and diversity in both digesta- and mucosa-associated intestinal microbiota, mucosa-associated intestinal microbiota seems more resilient to variations in the diet composition. To fully unveil the response of intestinal microbiota to dietary changes, concurrent profiling of digesta- and mucosa-associated intestinal microbiota is recommended whenever feasible. Specific taxa enriched in the intestinal mucosa are associated to gene expression related to immune responses and barrier function. Detailed studies are needed on the ecological and functional significance of taxa associated to intestinal microbiota dwelling on the mucosa.

Clubroot in Brassica: Recent advances in genomics, breeding and disease management

Genome ◽  
2021 ◽  
Author(s):  
Muhammad Jakir Hasan ◽  
Swati Megha ◽  
Habibur Rahman
Keyword(s):  
Host Resistance ◽  
Molecular Basis ◽  
Host Plants ◽  
Cultural Practices ◽  
Plasmodiophora Brassicae ◽  
Genetic Resistance ◽  
Vegetable Production ◽  
Comprehensive Understanding ◽  
Clubroot Disease

Clubroot disease, caused by Plasmodiophora brassicae, affects Brassica oilseed and vegetable production worldwide. This review is focused on various aspects of clubroot disease and its management, including understanding the pathogen and resistance in the host plants. Advances in genetics, molecular biology techniques and ‘omics’ research have helped to identify several major loci, QTL and genes from the Brassica genomes involved in the control of clubroot resistance. Transcriptomic studies have helped to extend our understanding of the mechanism of infection by the pathogen and the molecular basis of resistance/susceptibility in the host plants. A comprehensive understanding of the clubroot disease and host resistance would allow developing a better strategy by integrating the genetic resistance with cultural practices to manage this disease from a long-term perspective.

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