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Tanja Strive - One of the best experts on this subject based on the ideXlab platform.
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genomic insights into a population of introduced european rabbits oryctolagus cuniculus in australia and the development of Genetic Resistance to rabbit hemorrhagic disease virus rhdv
Transboundary and Emerging Diseases, 2021Co-Authors: S Metcalfe, S Elfekih, Tom Walsh, Tarnya Cox, Tanja StriveAbstract:The European rabbit (Oryctolagus cuniculus) is one of the most devastating invasive species in Australia. Since the 1950s, myxoma virus (MYXV) and Rabbit Hemorrhagic Disease Virus (RHDV) have been used to manage overabundant rabbit populations. Resistance to MYXV was observed within a few years of the release. More recently, Resistance to lethal RHDV infection has also been reported, undermining the efficiency of landscape-scale rabbit control. Previous studies suggest that Genetic Resistance to lethal RHDV infection may differ locally between populations, yet the mechanisms of Genetic Resistance remain poorly understood. Here, we used genotyping by sequencing (GBS) data representing a reduced representation of the genome, to investigate Australian rabbit populations. Our aims were to understand the relationship between populations and identify possible genomic signatures of selection for RHDV Resistance. One population we investigated had previously been reported to show levels of Resistance to lethal RHDV infection. This population was compared to three other populations with lower or no previously reported RHDV Resistance. We identified a set of novel candidate genes that could be involved in host-pathogen interactions such as virus binding and infection processes. These genes did not overlap with previous studies on RHDV Resistance carried out in different rabbit populations, suggesting that multiple mechanisms are feasible. These findings provide useful insights into the different potential mechanisms of Genetic Resistance to RHDV virus which will inform future functional studies in this area.
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increased virulence of rabbit haemorrhagic disease virus associated with Genetic Resistance in wild australian rabbits oryctolagus cuniculus
Virology, 2014Co-Authors: Peter Elsworth, John Kovaliski, Brian Cooke, Tanja Strive, Edward C Holmes, Ronald SinclairAbstract:The release of myxoma virus (MYXV) and Rabbit Haemorrhagic Disease Virus (RHDV) in Australia with the aim of controlling overabundant rabbits has provided a unique opportunity to study the initial spread and establishment of emerging pathogens, as well as their co-evolution with their mammalian hosts. In contrast to MYXV, which attenuated shortly after its introduction, rapid attenuation of RHDV has not been observed. By studying the change in virulence of recent field isolates at a single field site we show, for the first time, that RHDV virulence has increased through time, likely because of selection to overcome developing Genetic Resistance in Australian wild rabbits. High virulence also appears to be favoured as rabbit carcasses, rather than diseased animals, are the likely source of mechanical insect transmission. These findings not only help elucidate the co-evolutionary interaction between rabbits and RHDV, but reveal some of the key factors shaping virulence evolution.
Ross D Houston - One of the best experts on this subject based on the ideXlab platform.
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characterising the mechanisms underlying Genetic Resistance to amoebic gill disease in atlantic salmon using rna sequencing
BMC Genomics, 2020Co-Authors: Diego Robledo, A Hamilton, Alejandro P Gutierrez, James E Bron, Ross D HoustonAbstract:Gill 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. Comparison between resistant and susceptible animals primarily highlighted 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 pointed to a contrast in Th2 and Th17 responses, which is 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. In 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.
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characterising the mechanisms underlying Genetic Resistance to amoebic gill disease in atlantic salmon using rna sequencing
bioRxiv, 2019Co-Authors: Diego Robledo, A Hamilton, Alejandro P Gutierrez, James E Bron, Ross D HoustonAbstract:ABSTRACT Background Gill 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. Results Comparison 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. Conclusions In 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.
Jiuzhou Song - One of the best experts on this subject based on the ideXlab platform.
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genome wide identification of copy number variations between two chicken lines that differ in Genetic Resistance to marek s disease
BMC Genomics, 2015Co-Authors: Yiyuan Yan, Ning Yang, Hans H Cheng, Jiuzhou SongAbstract:Copy number variation (CNV) is a major source of genome polymorphism that directly contributes to phenotypic variation such as Resistance to infectious diseases. Lines 63 and 72 are two highly inbred experimental chicken lines that differ greatly in susceptibility to Marek’s disease (MD), and have been used extensively in efforts to identify the Genetic and molecular basis for Genetic Resistance to MD. Using next generation sequencing, we present a genome-wide assessment of CNVs that are potentially associated with Genetic Resistance to MD. Three chickens randomly selected from each line were sequenced to an average depth of 20×. Two popular software, CNVnator and Pindel, were used to call genomic CNVs separately. The results were combined to obtain a union set of genomic CNVs in the two chicken lines. A total of 5,680 CNV regions (CNVRs) were identified after merging the two datasets, of which 1,546 and 1,866 were specific to the MD resistant or susceptible line, respectively. Over half of the line-specific CNVRs were shared by 2 or more chickens, reflecting the reduced diversity in both inbred lines. The CNVRs fixed in the susceptible lines were significantly enriched in genes involved in MAPK signaling pathway. We also found 67 CNVRs overlapping with 62 genes previously shown to be strong candidates of the underlying genes responsible for the susceptibility to MD. Our findings provide new insights into the Genetic architecture of the two chicken lines and additional evidence that MAPK signaling pathway may play an important role in host response to MD virus infection. The rich source of line-specific CNVs is valuable for future disease-related association studies in the two chicken lines.
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marek s disease virus infection induces widespread differential chromatin marks in inbred chicken lines
BMC Genomics, 2012Co-Authors: Apratim Mitra, Juan Luo, Huanming Zhang, Kairong Cui, Keji Zhao, Jiuzhou SongAbstract:Marek’s disease (MD) is a neoplastic disease in chickens caused by the MD virus (MDV). Successful vaccine development against MD has resulted in increased virulence of MDV and the understanding of Genetic Resistance to the disease is, therefore, crucial to long-term control strategies. Also, epiGenetic factors are believed to be one of the major determinants of disease response. Here, we carried out comprehensive analyses of the epiGenetic landscape induced by MDV, utilizing genome-wide histone H3 lysine 4 and lysine 27 trimethylation maps from chicken lines with varying Resistance to MD. Differential chromatin marks were observed on genes previously implicated in the disease such as MX1 and CTLA-4 and also on genes reported in other cancers including IGF2BP1 and GAL. We detected bivalent domains on immune-related transcriptional regulators BCL6, CITED2 and EGR1, which underwent dynamic changes in both lines as a result of MDV infection. In addition, putative roles for GAL in the mechanism of MD progression were revealed. Our results confirm the presence of widespread epiGenetic differences induced by MD in chicken lines with different levels of Genetic Resistance. A majority of observed epiGenetic changes were indicative of increased levels of viral infection in the susceptible line symptomatic of lowered immunocompetence in these birds caused by early cytolytic infection. The GAL system that has known anti-proliferative effects in other cancers is also revealed to be potentially involved in MD progression. Our study provides further insight into the mechanisms of MD progression while revealing a complex landscape of epiGenetic regulatory mechanisms that varies depending on host factors.
James D Kelly - One of the best experts on this subject based on the ideXlab platform.
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characterization of the Genetic Resistance to colletotrichum lindemuthianum in common bean differential cultivars
Plant Disease, 1996Co-Authors: R A Young, James D KellyAbstract:The inheritance of Genetic Resistance to bean anthracnose in genotypes Catrachita and SEL 1360 derived from two anthracnose differential cultivars, AB 136 and G 2333, respectively, is described. Segregation data from three different F2 populations and their respective F 2:3 families indicated that a single dominant gene is responsible for the anthracnose Resistance in Catrachita. In the test for allelism, chi-square test confirmed that the single dominant Resistance gene in Catrachita was situated at a different locus from previously characterized Resistance genes A, Are, Mexique 1, Mexique 2, and Mexique 3. It is proposed that the single dominant Resistance gene present in Catrachita be assigned the Genetic symbol Co-6, Co for Colletotrichum and 6 because it is the sixth major anthracnose Resistance gene characterized and reported in the literature. Segregation in the three F2 populations where SEL 1360 was used as the resistant parent fitted a 3:1 (R-:rr) ratio and a 1:2:1 (RR:Rr:rr) ratio in the F 2:3 families. Segregation data suggested that a single dominant gene was conditioning Resistance to anthracnose in SEL 1360. The test for allelism involving SEL 1360 indicated that the single dominant gene in SEL 1360 is independent from A (Co-1), Are (Co-2), Mexique 1 (Co-3), and Mexique 2 (Co-4) genes. However, the dominant gene in SEL 1360 did not segregate independently from the Resistance gene Mexique 3 in the differential cultivar TU, demonstrating that both dominant alleles are located at the same locus. Deployment of major genes of Middle American origin, such as Co-6 and Mexique 3 (Co-5), in different combinations with other characterized genes of Andean origin is possible and should contribute to more durable anthracnose Resistance in common bean.
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identification and potential use of a molecular marker for rust Resistance in common bean
Theoretical and Applied Genetics, 1993Co-Authors: Phillip N Miklas, J R Stavely, James D KellyAbstract:Summary. The Up2 gene of common bean (PhaseoIus vulgaris L.) is an important source of dominant Genetic Resistance to the bean rust pathogen [ Uromyces appendiculatus (Pers. ex Pers.) Unger var 'appendiculatus' [syn U. phaseoli (Reben) Wint.]. Up2 in combination with other rust Resistance genes may be used to obtain potentially stable Genetic Resistance. It is difficult, however, to combine rust Resistance genes effective against a single race due to epistatic interactions that frequently occur between them. A strategy that employed bulked DNA samples formed separately from the DNA of three BC6F 2 individuals with Up2 and three without Up2 as contrasting near-isogenic lines (NILs) was used to identify random amplified polymorphic DNA fragments (RAPDs) tightly linked to the Up2 locus. Only 1 of 931 fragments amplified by 167 10-mer primers of arbitrary sequence in the polymerase chain reaction (PCR) was polymorphic. The RAPD marker (OA14110o) amplified by the 5'TCTGTGCTGG-3' primer was repeatable and its presence and absence easy to score. No recombination was observed between OA1411oo and the dominant Upz allele within a segregating BC6F 2 population of 84 individuals. This result suggests that OA141 loo and Up2 are tightly linked. Andean and Mesoamerican bean germ plasm, with and without the Up2 allele, were assayed for the presence of OA141 loo. Apparently, the marker is of Andean origin because all Andean lines, with or without the Upz allele, contained the marker,
Diego Robledo - One of the best experts on this subject based on the ideXlab platform.
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characterising the mechanisms underlying Genetic Resistance to amoebic gill disease in atlantic salmon using rna sequencing
BMC Genomics, 2020Co-Authors: Diego Robledo, A Hamilton, Alejandro P Gutierrez, James E Bron, Ross D HoustonAbstract:Gill 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. Comparison between resistant and susceptible animals primarily highlighted 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 pointed to a contrast in Th2 and Th17 responses, which is 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. In 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.
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characterising the mechanisms underlying Genetic Resistance to amoebic gill disease in atlantic salmon using rna sequencing
bioRxiv, 2019Co-Authors: Diego Robledo, A Hamilton, Alejandro P Gutierrez, James E Bron, Ross D HoustonAbstract:ABSTRACT Background Gill 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. Results Comparison 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. Conclusions In 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.