The Experts below are selected from a list of 210 Experts worldwide ranked by ideXlab platform
S. H. Phua - One of the best experts on this subject based on the ideXlab platform.
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towards genomic selection for Facial Eczema disease tolerance in the new zealand sheep industry
Animal Genetics, 2014Co-Authors: S. H. Phua, J C Mcewan, D L Hyndman, Hayley Baird, Benoit Auvray, Michael Lee, K. G. DoddsAbstract:Summary Pithomycotoxicosis, more commonly known as Facial Eczema (FE), is a liver disease that occurs predominantly in New Zealand because of its toxigenic Pithomyces chartarum strains. The first reported case was in sheep in 1887. Since the 1930s, a number of studies have been conducted in an attempt to mitigate the problems FE has on the sheep and dairy industries. The research in these studies included work on fungicide and biological control of the saprophytic fungus, use of different pasture plants to inhibit fungal growth, stock management with respect to pasture fungal spore counts and the use of zinc prophylaxis on animals. The finding that there was a genetic basis in FE sensitivity in sheep prompted research for a genetic approach to mitigation in the form of a diagnostic DNA test for susceptibility to the disease. Recently, we have used the Illumina OvineSNP50 BeadChip to develop a genome-enabled prediction approach to screen for FE-tolerant sheep. Our current best genomic prediction for FE is for the Romney breed and has an accuracy of 0.38. This prediction accuracy is not as high as the individual accuracy gained by an artificial challenge test (0.64). However, it has the advantage of being a non-invasive test and can be provided as part of genomic testing for other traits at minimal cost.
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identifying chromosomal selection sweep regions in Facial Eczema selection line animals using an ovine 50k snp array
Animal Genetics, 2014Co-Authors: S. H. Phua, Hayley Baird, Rudiger Brauning, K. G. DoddsAbstract:Summary Facial Eczema (FE) is a hepato-mycotoxicosis found mainly in New Zealand sheep and cattle. When genetics was found to be a factor in FE susceptibility, resistant and susceptible selection lines of Romney sheep were established to enable further investigations of this disease trait. Using the Illumina OvineSNP50 BeadChip, we conducted a selection-sweep experiment on these FE genetic lines. Two analytical methods were used to detect selection signals, namely the Peddrift test (Dodds & McEwan, 1997) and fixation index FST (Weir & Hill, 2002). Of 50 975 single nucleotide polymorphism (SNP) markers tested, there were three that showed highly significant allele frequency differences between the resistant and susceptible animals (Peddrift nominal P < 0.000001). These SNP loci are located on chromosomes OAR1, OAR11 and OAR12 that coincide precisely with the three highest genomic FST peaks. In addition, there are nine less significant Peddrift SNPs (nominal P ≤ 0.000009) on OAR6 (n = 2), OAR9 (n = 2), OAR12, OAR19 (n = 2), OAR24 and OAR26. In smoothed FST (five-SNP moving average) plots, the five most prominent peaks are on OAR1, OAR6, OAR7, OAR13 and OAR19. Although these smoothed FST peaks do not coincide with the three most significant Peddrift SNP loci, two (on OAR6 and OAR19) overlap with the set of less significant Peddrift SNPs above. Of these 12 Peddrift SNPs and five smoothed FST regions, none is close to the FE candidate genes catalase and ABCG2; however, two on OAR1 and one on OAR13 fall within suggestive quantitative trait locus regions identified in a previous genome screen experiment. The present studies indicated that there are at least eight genomic regions that underwent a selection sweep in the FE lines.
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review of genetic studies of susceptibility to Facial Eczema in sheep and dairy cattle
New Zealand Journal of Agricultural Research, 2013Co-Authors: C. A. Morris, S. H. Phua, N G Cullen, Neale R. TowersAbstract:Abstract Genetic responses of sheep and dairy cattle to the hepatic mycotoxin, sporidesmin, were reviewed. The mycotoxin can lead to clinical Facial Eczema (FE) in the most susceptible and severely challenged animals. The extent of hepatic injury is normally assessed from an enzyme secreted into the blood, gamma-glutamyltransferase (GGT). Latest heritability estimates for the natural logarithm of GGT level, 21 days or more after a sporidesmin challenge, were 0.45±0.03 in sheep and 0.34±0.02 in dairy cattle. Clinical FE follows from phylloerythrin (from chlorophyll) spilling over from the bile duct. Upon exposure to sunlight, phylloerythrin absorbs ultraviolet radiation, becoming reactive. Neither its concentration in blood nor clinical cases of FE are likely to be good indicators of liver damage from FE for ranking sires. Gaps in knowledge about genetic factors relating to FE susceptibility are highlighted.
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A preliminary study on breed differences in susceptibility of sheep to mycotoxin sporidesmin.
2013Co-Authors: S. H. Phua, H. Henry, K. G. Dodds, N. L. VillalobosAbstract:Sporidesmin is the mycotoxin that causes Facial Eczema disease (FE) in New Zealand (NZ) livestock. In an artificial sporidesmin dosing test, the introduced Finnish Landrace sheep breed was found to be significantly more tolerant to FE than the introduced Texel breed. This finding enables cross-breeding strategies to improve disease tolerance. Combining published data with the current study, a tentative inference is that Finnish Landrace, Merino and East Friesian are more FE resistant than Romney, Texel and Border Leicester.
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a genome screen experiment to detect quantitative trait loci affecting resistance to Facial Eczema disease in sheep
Animal Genetics, 2009Co-Authors: S. H. Phua, N. R. Towers, C. A. Morris, K. G. Dodds, H G Garmonsway, Hm Henry, A E Beattie, A M CrawfordAbstract:Summary Facial Eczema (FE) is a secondary photosensitization disease arising from liver cirrhosis caused by the mycotoxin sporidesmin. The disease affects sheep, cattle, deer and goats, and costs the New Zealand sheep industry alone an estimated NZ$63M annually. A long-term sustainable solution to this century-old FE problem is to breed for disease-resistant animals by marker-assisted selection. As a step towards finding a diagnostic DNA test for FE sensitivity, we have conducted a genome-scan experiment to screen for quantitative trait loci (QTL) affecting this trait in Romney sheep. Four F1 sires, obtained from reciprocal matings of FE resistant and susceptible selection-line animals, were used to generate four outcross families. The resulting half-sib progeny were artificially challenged with sporidesmin to phenotype their FE traits measured in terms of their serum levels of liver-specific enzymes, namely gamma-glutamyl transferase and glutamate dehydrogenase. In a primary screen using selective genotyping on extreme progeny of each family, a total of 244 DNA markers uniformly distributed over all 26 ovine autosomes (with an autosomal genome coverage of 79–91%) were tested for linkage to the FE traits. Data were analysed using Haley–Knott regression. The primary screen detected one significant and one suggestive QTL on chromosomes 3 and 8 respectively. Both the significant and suggestive QTL were followed up in a secondary screen where all progeny were genotyped and analysed; the QTL on chromosome 3 was significant in this analysis.
C. A. Morris - One of the best experts on this subject based on the ideXlab platform.
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review of genetic studies of susceptibility to Facial Eczema in sheep and dairy cattle
New Zealand Journal of Agricultural Research, 2013Co-Authors: C. A. Morris, S. H. Phua, N G Cullen, Neale R. TowersAbstract:Abstract Genetic responses of sheep and dairy cattle to the hepatic mycotoxin, sporidesmin, were reviewed. The mycotoxin can lead to clinical Facial Eczema (FE) in the most susceptible and severely challenged animals. The extent of hepatic injury is normally assessed from an enzyme secreted into the blood, gamma-glutamyltransferase (GGT). Latest heritability estimates for the natural logarithm of GGT level, 21 days or more after a sporidesmin challenge, were 0.45±0.03 in sheep and 0.34±0.02 in dairy cattle. Clinical FE follows from phylloerythrin (from chlorophyll) spilling over from the bile duct. Upon exposure to sunlight, phylloerythrin absorbs ultraviolet radiation, becoming reactive. Neither its concentration in blood nor clinical cases of FE are likely to be good indicators of liver damage from FE for ranking sires. Gaps in knowledge about genetic factors relating to FE susceptibility are highlighted.
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a genome screen experiment to detect quantitative trait loci affecting resistance to Facial Eczema disease in sheep
Animal Genetics, 2009Co-Authors: S. H. Phua, N. R. Towers, C. A. Morris, K. G. Dodds, H G Garmonsway, Hm Henry, A E Beattie, A M CrawfordAbstract:Summary Facial Eczema (FE) is a secondary photosensitization disease arising from liver cirrhosis caused by the mycotoxin sporidesmin. The disease affects sheep, cattle, deer and goats, and costs the New Zealand sheep industry alone an estimated NZ$63M annually. A long-term sustainable solution to this century-old FE problem is to breed for disease-resistant animals by marker-assisted selection. As a step towards finding a diagnostic DNA test for FE sensitivity, we have conducted a genome-scan experiment to screen for quantitative trait loci (QTL) affecting this trait in Romney sheep. Four F1 sires, obtained from reciprocal matings of FE resistant and susceptible selection-line animals, were used to generate four outcross families. The resulting half-sib progeny were artificially challenged with sporidesmin to phenotype their FE traits measured in terms of their serum levels of liver-specific enzymes, namely gamma-glutamyl transferase and glutamate dehydrogenase. In a primary screen using selective genotyping on extreme progeny of each family, a total of 244 DNA markers uniformly distributed over all 26 ovine autosomes (with an autosomal genome coverage of 79–91%) were tested for linkage to the FE traits. Data were analysed using Haley–Knott regression. The primary screen detected one significant and one suggestive QTL on chromosomes 3 and 8 respectively. Both the significant and suggestive QTL were followed up in a secondary screen where all progeny were genotyped and analysed; the QTL on chromosome 3 was significant in this analysis.
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sheep selected for resistance to Facial Eczema disease also show higher tolerance to acetaminophen challenge
Matching genetics and environment: a new look at an old topic. Proceedings of the 18th Conference of the Association for the Advancement of Animal Bre, 2009Co-Authors: S. H. Phua, H. Henry, P Johnstone, A Findlay, C. A. MorrisAbstract:Facial Eczema disease (FE) is a hepato-mycotoxicosis caused by sporidesmin, leading to secondary photosensitisation in severely affected sheep and cattle. Two genetic lines of Romney are maintained by selection for resistance and susceptibility to FE. Five groups of 8 animals, each group composed of 4 animals from each line, were artificially challenged with different dose rates (25, 50, 75, 150 & 250 mg/kg liveweight) of acetaminophen (or paracetamol). Weekly blood samples were collected from each animal for 5 weeks after dosing and were used for liver function tests (glutamate dehydrogenase (GDH), gamma-glutamyl transferase (GGT), bilirubin and albumin/globulin ratio) to measure their liver injury. The results showed that FE resistant-line animals were more tolerant of acetaminophen than the susceptible-line animals, and that they also recovered faster after the drug challenge.
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testing glutathione s transferase for an association with Facial Eczema resistance in cattle
Proceedings of the New Zealand Society of Animal Production, 2007Co-Authors: C. A. Morris, N G Cullen, R. MundayAbstract:Resistance to Facial Eczema (FE) in cattle is known to be a heritable trait. The commonly used indicators of susceptibility in affected groups of animals are gamma glutamyl-transferase (GGT) and glutamate dehydrogenase (GDH), which indicate the severity of the liver injury associated with FE. Published research using mouse models suggests that glutathione-S-transferase (GST) may be a downstream indicator of variation in FE susceptibility, and a study was carried out in calves to test this. Friesian-sired and Jerseysired bull calves were purchased from dairy herds in spring 2004, artificially reared from about four days of age, weaned at 75-80 kg, monitored for base-line GGT activity in blood, and then dosed orally with sporidesmin. At 14 and 21 days after dosing, blood samples were taken to measure the activities of both GDH and GGT. A sample of 45 Friesian calves and 45 Jersey calves from the high and low outliers (using GDH activity within breed, 14 days after dosing) were blood-sampled 15 or 16 days after dosing and measured for GST activity, with 20-25 animals sampled each day, in balanced groups. There were significant differences in GST activity between high and low GDH groups (P < 0.01), and the pooled within-analysisday regression of GST activity on logGGT activity (day 21) was negative (P < 0.05). Results confirmed that low erythrocytic GST activity is an indicator of FE susceptibility, although the differences seen between resistant and susceptible animals are insufficient for use as a predictive tool.
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genetic parameters for resistance to Facial Eczema in dairy cattle
Proceedings of the New Zealand Society of Animal Production, 2006Co-Authors: N G Cullen, C. A. Morris, S M HickeyAbstract:A project was designed to progeny-test dairy industry sires for their resistance to Facial Eczema (FE), as a preliminary step towards identifying DNA markers or genes for FE resistance. The FE disease is caused by the toxin, sporidesmin, produced by spores of a fungus, Pithomyces chartarum, found on many pastures in summer and autumn in the North Island of New Zealand. In susceptible animals, sporidesmin causes liver injury, and the cost of FE to the dairy industry is measured in tens of millions of dollars in years with serious outbreaks ($3.6 to 66.2M per annum). Earlier studies in New Zealand have established that resistance to FE in cattle is a heritable trait, with resistance measured by variation in activity in blood of liver-derived enzymes, gamma-glutamyltransferase (GGT) and the associated glutamate dehydrogenase (GDH). Widelyused Friesian and Jersey sires were progeny-tested via 572 specially-reared sons (born in 2002-04 and dosed with sporidesmin), and also via 3761 daughters in autumns 2004 and 2005 in 17 herds with 3-22% clinical cases of FE per herd. The data were combined from all sources, including four earlier years of GGT records (1173 animals born in the 1986, 1989, 1990 and 1992 birth years), and standardisation was applied to each contemporary group. Heritabilities were estimated for Friesians (0.47 ± 0.07 for log GGT; 0.32 ± 0.08 for log GDH) and for Jerseys (0.37 ± 0.06 and 0.39 ± 0.09, respectively), and there was a very high genetic correlation between activities of the two enzymes (0.93 ± 0.03). Sixty-eight sires had reliabilities of >0.70 for log GGT Breeding Value and 71 others had reliabilities between 0.60 and 0.70. The sires progeny-tested Proceedings of the New Zealand Society of Animal Production 2006, Vol 66 311 in this way generally were already proven for dairy traits and had been widely used, so that FE selection among these sires would be an additional trait when they were already old. Alternative approaches would be to performance-test young bulls for FE resistance, or to use sire and progeny data and their DNA to identify DNA markers or genes for FE resistance.
K. G. Dodds - One of the best experts on this subject based on the ideXlab platform.
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towards genomic selection for Facial Eczema disease tolerance in the new zealand sheep industry
Animal Genetics, 2014Co-Authors: S. H. Phua, J C Mcewan, D L Hyndman, Hayley Baird, Benoit Auvray, Michael Lee, K. G. DoddsAbstract:Summary Pithomycotoxicosis, more commonly known as Facial Eczema (FE), is a liver disease that occurs predominantly in New Zealand because of its toxigenic Pithomyces chartarum strains. The first reported case was in sheep in 1887. Since the 1930s, a number of studies have been conducted in an attempt to mitigate the problems FE has on the sheep and dairy industries. The research in these studies included work on fungicide and biological control of the saprophytic fungus, use of different pasture plants to inhibit fungal growth, stock management with respect to pasture fungal spore counts and the use of zinc prophylaxis on animals. The finding that there was a genetic basis in FE sensitivity in sheep prompted research for a genetic approach to mitigation in the form of a diagnostic DNA test for susceptibility to the disease. Recently, we have used the Illumina OvineSNP50 BeadChip to develop a genome-enabled prediction approach to screen for FE-tolerant sheep. Our current best genomic prediction for FE is for the Romney breed and has an accuracy of 0.38. This prediction accuracy is not as high as the individual accuracy gained by an artificial challenge test (0.64). However, it has the advantage of being a non-invasive test and can be provided as part of genomic testing for other traits at minimal cost.
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identifying chromosomal selection sweep regions in Facial Eczema selection line animals using an ovine 50k snp array
Animal Genetics, 2014Co-Authors: S. H. Phua, Hayley Baird, Rudiger Brauning, K. G. DoddsAbstract:Summary Facial Eczema (FE) is a hepato-mycotoxicosis found mainly in New Zealand sheep and cattle. When genetics was found to be a factor in FE susceptibility, resistant and susceptible selection lines of Romney sheep were established to enable further investigations of this disease trait. Using the Illumina OvineSNP50 BeadChip, we conducted a selection-sweep experiment on these FE genetic lines. Two analytical methods were used to detect selection signals, namely the Peddrift test (Dodds & McEwan, 1997) and fixation index FST (Weir & Hill, 2002). Of 50 975 single nucleotide polymorphism (SNP) markers tested, there were three that showed highly significant allele frequency differences between the resistant and susceptible animals (Peddrift nominal P < 0.000001). These SNP loci are located on chromosomes OAR1, OAR11 and OAR12 that coincide precisely with the three highest genomic FST peaks. In addition, there are nine less significant Peddrift SNPs (nominal P ≤ 0.000009) on OAR6 (n = 2), OAR9 (n = 2), OAR12, OAR19 (n = 2), OAR24 and OAR26. In smoothed FST (five-SNP moving average) plots, the five most prominent peaks are on OAR1, OAR6, OAR7, OAR13 and OAR19. Although these smoothed FST peaks do not coincide with the three most significant Peddrift SNP loci, two (on OAR6 and OAR19) overlap with the set of less significant Peddrift SNPs above. Of these 12 Peddrift SNPs and five smoothed FST regions, none is close to the FE candidate genes catalase and ABCG2; however, two on OAR1 and one on OAR13 fall within suggestive quantitative trait locus regions identified in a previous genome screen experiment. The present studies indicated that there are at least eight genomic regions that underwent a selection sweep in the FE lines.
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A preliminary study on breed differences in susceptibility of sheep to mycotoxin sporidesmin.
2013Co-Authors: S. H. Phua, H. Henry, K. G. Dodds, N. L. VillalobosAbstract:Sporidesmin is the mycotoxin that causes Facial Eczema disease (FE) in New Zealand (NZ) livestock. In an artificial sporidesmin dosing test, the introduced Finnish Landrace sheep breed was found to be significantly more tolerant to FE than the introduced Texel breed. This finding enables cross-breeding strategies to improve disease tolerance. Combining published data with the current study, a tentative inference is that Finnish Landrace, Merino and East Friesian are more FE resistant than Romney, Texel and Border Leicester.
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a genome screen experiment to detect quantitative trait loci affecting resistance to Facial Eczema disease in sheep
Animal Genetics, 2009Co-Authors: S. H. Phua, N. R. Towers, C. A. Morris, K. G. Dodds, H G Garmonsway, Hm Henry, A E Beattie, A M CrawfordAbstract:Summary Facial Eczema (FE) is a secondary photosensitization disease arising from liver cirrhosis caused by the mycotoxin sporidesmin. The disease affects sheep, cattle, deer and goats, and costs the New Zealand sheep industry alone an estimated NZ$63M annually. A long-term sustainable solution to this century-old FE problem is to breed for disease-resistant animals by marker-assisted selection. As a step towards finding a diagnostic DNA test for FE sensitivity, we have conducted a genome-scan experiment to screen for quantitative trait loci (QTL) affecting this trait in Romney sheep. Four F1 sires, obtained from reciprocal matings of FE resistant and susceptible selection-line animals, were used to generate four outcross families. The resulting half-sib progeny were artificially challenged with sporidesmin to phenotype their FE traits measured in terms of their serum levels of liver-specific enzymes, namely gamma-glutamyl transferase and glutamate dehydrogenase. In a primary screen using selective genotyping on extreme progeny of each family, a total of 244 DNA markers uniformly distributed over all 26 ovine autosomes (with an autosomal genome coverage of 79–91%) were tested for linkage to the FE traits. Data were analysed using Haley–Knott regression. The primary screen detected one significant and one suggestive QTL on chromosomes 3 and 8 respectively. Both the significant and suggestive QTL were followed up in a secondary screen where all progeny were genotyped and analysed; the QTL on chromosome 3 was significant in this analysis.
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Cloning, mapping and association studies of the ovine ABCG2 gene with Facial Eczema disease in sheep
'Wiley', 2007Co-Authors: Ej Duncan, K. G. Dodds, Hm Henry, Mp Thompson, S. H. PhuaAbstract:Facial Eczema (FE) is a hepatogenous mycotoxicosis in sheep caused by the fungal toxin sporidesmin. Resistance to FE is a multigenic trait. To identify QTL associated with this trait, a scan of ovine chromosomes was implemented. In addition, ABCG2 was investigated as a possible positional candidate gene because of its sequence homology to the yeast PDR5 protein and its functional role as a xenobiotic transporter. The sequence of ovine ABCG2 cDNA was obtained from liver mRNA by RT‐PCR and 5′ and 3′ RACE. The predicted protein sequence shares >80% identity with other mammalian ABCG2 proteins. SNPs were identified within exon 6, exon 9 and intron 4. The intron 4 SNP was used to map ABCG2 to ovine chromosome 6 (OAR6), about 2 cM distal to microsatellite marker OarAE101. Interestingly, this chromosomal region contains weak evidence for a FE QTL detected in a previous genome‐scan experiment. To further investigate the association of ABCG2 with FE, allele frequencies for the three SNPs plus three neighbouring microsatellite markers were tested for differences in sheep selected for and against FE. Significant differences were detected in the allele frequencies of the intronic SNP marker among the resistant, susceptible and control lines. No difference in the levels of ABCG2 expression between the resistant and susceptible animals was detected by Northern hybridisation of liver RNA samples. However, significantly higher expression was observed in sporidesmin‐dosed sheep compared with naïve animals. Our inference is that the ABCG2 gene may play a minor role in FE sensitivity in sheep, at least within these selection lines
Neale R. Towers - One of the best experts on this subject based on the ideXlab platform.
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review of genetic studies of susceptibility to Facial Eczema in sheep and dairy cattle
New Zealand Journal of Agricultural Research, 2013Co-Authors: C. A. Morris, S. H. Phua, N G Cullen, Neale R. TowersAbstract:Abstract Genetic responses of sheep and dairy cattle to the hepatic mycotoxin, sporidesmin, were reviewed. The mycotoxin can lead to clinical Facial Eczema (FE) in the most susceptible and severely challenged animals. The extent of hepatic injury is normally assessed from an enzyme secreted into the blood, gamma-glutamyltransferase (GGT). Latest heritability estimates for the natural logarithm of GGT level, 21 days or more after a sporidesmin challenge, were 0.45±0.03 in sheep and 0.34±0.02 in dairy cattle. Clinical FE follows from phylloerythrin (from chlorophyll) spilling over from the bile duct. Upon exposure to sunlight, phylloerythrin absorbs ultraviolet radiation, becoming reactive. Neither its concentration in blood nor clinical cases of FE are likely to be good indicators of liver damage from FE for ranking sires. Gaps in knowledge about genetic factors relating to FE susceptibility are highlighted.
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antioxidants in blood from sheep lines divergently selected for Facial Eczema resistance
New Zealand Journal of Agricultural Research, 2004Co-Authors: W D Hohenboken, Neale R. Towers, R. Munday, C. A. Morris, N. C. Amyes, G De Nicolo, S. H. PhuaAbstract:Abstract Romney sheep have been evaluated for resistance to Facial Eczema (FE) using a process which involves challenge with the FE toxin, sporidesmin, and they have been bred in selection lines for increased resistance (R) or susceptibility (S) to FE. There is evidence that sporidesmin exerts its toxic effects by generating reactive oxygen species, and protection can be afforded by a number of antioxidants and antioxidant enzymes. Our objective was to summarise three separate experiments to determine whether the R and S lines differed in antioxidant mechanisms, in search of a non‐invasive genetic marker. Lines were compared for the activities of four enzymes in blood in Experiment 1, superoxide dismutase (SOD), catalase (CAT), glu‐tathione peroxidase (GPX), and glutathione reduct‐ase (GR), and for the concentration of the tri‐peptide thiol, glutathione (GSH). SOD, CAT, and GSH were also recorded in Experiment 2, and GPX alone in Experiment 3. Heritabilities were estimated for SOD, CAT, and GSH. SOD activ...
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A zinc-containing intraruminal device for prevention of the sporidesmin-induced cholangiopathy of Facial Eczema in calves.
New Zealand Veterinary Journal, 2001Co-Authors: Rex Munday, Neale R. Towers, A.m. Thompson, Barry L. Smith, K. O'donnell, R.m. Mcdonald, M. StirnemannAbstract:Abstract Aim: To develop and evaluate a zinc-containing intraruminal controlled-release bolus for protection of calves (175 – 250 kg bodyweight) against Facial Eczema (FE). Methods: Boluses releasing zinc, in the form of zinc oxide, at rates ranging from 1.67 to 4.25 g/day were administered to calves which were challenged 4 weeks later with the FE toxin, sporidesmin. The efficacy of the boluses in protecting against sporidesmin-induced cholangiopathy was determined by measuring serum activities of gamma-glutamyltransferase (GGT). Results: A bolus releasing zinc at approximately 4.25 g/day gave excellent protection against sporidesmin toxicity for periods of up to 5 weeks duration. Conclusions: This zinc-containing intraruminal controlled-release bolus has the potential to markedly reduce the incidence and severity of FE in calves within a 175 – 250 kg bodyweight range.
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susceptibility to Facial Eczema in lambs sired by east friesian romney control and romney Facial Eczema resistant rams
New Zealand Journal of Agricultural Research, 2001Co-Authors: C. A. Morris, C. Wesselink, J A Wilson, G Denicolo, Neale R. TowersAbstract:Abstract Ten East Friesian (EF), eight Romney Control (RC), and two Romney Facial Eczema Resistant (RR) rams were mated with Romney (R) ewes to generate EF × R, RC × R, and RR × R lambs. These lambs were compared for their susceptibility to an oral challenge with sporidesmin, the toxin causing Facial Eczema. All lambs of 16.0 kg or above (average weight 21.3 kg) were dosed after weaning with sporidesmin (0.14 mg kg‐1 liveweight) at an average age of 83 days. Resistance or susceptibility was assessed by taking a blood sample 21 days after challenge, and measuring serum gamma‐glutamyltransferase (GGT), an enzyme whose concentration is elevated after the liver injury resulting from a toxic challenge. In total, 289 animals were challenged (96, 119, and 74, respectively, for sire strains EF, RC, and RR). Percentages of non‐reactors with GGT concentrations below a threshold value indicative of subclinical Facial Eczema (<56 i.u. l‐1) were 62, 37, and 57 for sire strains EF, RC, and RR, respectively. The EF and ...
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correlated responses to selection for or against Facial Eczema susceptibility in romney sheep in new zealand
New Zealand Journal of Agricultural Research, 1999Co-Authors: C. A. Morris, Neale R. Towers, N. C. Amyes, C. WesselinkAbstract:Abstract Genetic selection for or against susceptibility to Facial Eczema (FE) in Romney sheep began in 1975, with the establishment of a resistant (R) selection flock, a susceptible (S) selection flock, and later (in 1982) a control (C) flock. For all but the initial years, rams were identified by performance testing with a sporidesmin challenge, then ranked on relative elevation of the liver enzyme, gamma glutamyltransferase (GGT), measured in serum. A different dose rate of sporidesmin was used for performance testing in the R and the S flocks, with a balanced half of the C‐flock animals being tested at each dose rate. Results are reported here up to the 1997‐born lamb crop. Mixed‐model animal‐model methods were used to determine the direct responses to selection, expressing results as breeding values for loge GGT. Correlated responses were monitored in lambs for weights, fleece weight, and survival, and in ewes for reproductive traits. Up to 1997, a 9‐fold difference in GGT concentration, 3 weeks afte...
N. R. Towers - One of the best experts on this subject based on the ideXlab platform.
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a genome screen experiment to detect quantitative trait loci affecting resistance to Facial Eczema disease in sheep
Animal Genetics, 2009Co-Authors: S. H. Phua, N. R. Towers, C. A. Morris, K. G. Dodds, H G Garmonsway, Hm Henry, A E Beattie, A M CrawfordAbstract:Summary Facial Eczema (FE) is a secondary photosensitization disease arising from liver cirrhosis caused by the mycotoxin sporidesmin. The disease affects sheep, cattle, deer and goats, and costs the New Zealand sheep industry alone an estimated NZ$63M annually. A long-term sustainable solution to this century-old FE problem is to breed for disease-resistant animals by marker-assisted selection. As a step towards finding a diagnostic DNA test for FE sensitivity, we have conducted a genome-scan experiment to screen for quantitative trait loci (QTL) affecting this trait in Romney sheep. Four F1 sires, obtained from reciprocal matings of FE resistant and susceptible selection-line animals, were used to generate four outcross families. The resulting half-sib progeny were artificially challenged with sporidesmin to phenotype their FE traits measured in terms of their serum levels of liver-specific enzymes, namely gamma-glutamyl transferase and glutamate dehydrogenase. In a primary screen using selective genotyping on extreme progeny of each family, a total of 244 DNA markers uniformly distributed over all 26 ovine autosomes (with an autosomal genome coverage of 79–91%) were tested for linkage to the FE traits. Data were analysed using Haley–Knott regression. The primary screen detected one significant and one suggestive QTL on chromosomes 3 and 8 respectively. Both the significant and suggestive QTL were followed up in a secondary screen where all progeny were genotyped and analysed; the QTL on chromosome 3 was significant in this analysis.
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inheritance of resistance to Facial Eczema a review of research findings from sheep and cattle in new zealand
New Zealand Veterinary Journal, 2004Co-Authors: C. A. Morris, B.l. Smith, N. R. Towers, W D Hohenboken, Nauman J Maqbool, S. H. PhuaAbstract:Facial Eczema (FE) is a costly problem to New Zealand pastoral agriculture, and has a detrimental impact on animal wellbeing. Incidence and severity of the disease can be reduced by grazing management and zinc prophylaxis. An additional strategy is to breed animals that are genetically resistant to intoxication with sporidesmin, the causative mycotoxin. This review summarises research findings on the inheritance of resistance of animals to FE, including evidence of among- and within-breed genetic variation, direct and correlated responses to selection, and identification of genetic markers and candidate genes for FE resistance.
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catalase gene is associated with Facial Eczema disease resistance in sheep
Animal Genetics, 1999Co-Authors: S. H. Phua, N. R. Towers, C. A. Morris, K. G. Dodds, K A Paterson, J C Mcewan, H G Garmonsway, A M CrawfordAbstract:Facial Eczema (FE) is a hepatogenous photosensitization disease of ruminant animals, particularly in sheep which vary widely in their susceptibility to the disease. The liver damage is caused by the mycotoxin, sporidesmin. There is evidence that the toxicity of sporidesmin is due to its ability to generate ‘active oxygen’ species. We evaluated the catalase gene, which encodes an enzyme with antioxidant functions, as a candidate for determining the susceptibility of sheep to the disease. Two microsatellite markers, OarSHP3 and OarSHP4, which flank the sheep catalase gene, were isolated from a Yeast Artificial Chromosome (YAC) clone. These markers mapped the catalase locus by linkage to ovine chromosome 15. Eleven informative markers spaced throughout chromosome 15, inclusive of the catalase marker OarSHP4, gave no significant linkage with the disease traits when analysed in four outcross resource pedigrees. However, OarSHP3 and OarSHP4 allele frequencies showed significant differences between FE resistant and susceptible selection-lines. Comparison of sequences of catalase cDNAs from sheep of resistant and susceptible lines showed only two silent mutations. A single nucleotide polymorphisms (KP1) in exon 6 of the catalase gene also showed significant differences in allele frequencies between the selection lines. The lack of evidence for linkage in outcross pedigrees, but the significant association in the genetic lines, implies that catalase is involved in determining the susceptibility of sheep to Facial Eczema, and that the candidate gene’s effect is probably recessive or minor.
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faecal nematode egg counts and Facial Eczema susceptibility in romneys
Proceedings of the New Zealand Society of Animal Production, 1996Co-Authors: C. A. Morris, N. R. Towers, N. C. Amyes, T G Watson, M Wheeler, B C HoskingAbstract:A study was carried out in two groups of flocks to estimate the relationship between susceptibility to Facial Eczema (FE) and susceptibility to nematode parasites. Faecal egg count (FEC) data on lambs born in 1989-92 from 53 sire groups were collected on the Ruakura Romney flocks which have been divergently selected for resistance/susceptibility to FE. In addition, the Romney flocks selected at Rotomahana/Tokanui Stations for resistance/susceptibility to FEC were sampled to provide the converse (i.e. FE data) on lambs born in 1988 and 1989, and representing 43 sires. Faecal samples for FEC were collected from lambs in January and March (separated by an anthelmintic treatment) and the FEC data were analysed using a loge transformation. FE susceptibilities, using the enzyme gamma-glutamyltransferase (GGT) as an indicator, were obtained in the FE flocks at Ruakura after an oral sporidesmin challenge in May, and in the FEC flocks at Tokanui after unintentional field challenge; the GGT data were also analysed using a loge transformation. The weighted average heritabilities of loge GGT and loge (FEC+100) were 0.44±0.03 and 0.33±0.05, respectively. At Ruakura, the two traits had a genetic correlation of 0.15±0.15, and at Tokanui, the corresponding correlation was 0.22±0.12, with a combined estimate of 0.19±0.09 (P<0.05). These results indicated that there was a tendency for the two traits to be positively associated among sire groups, when both types of challenge were applied in sequence.
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Competition of a sporidesmin-producing Pithomyces strain with a non-toxigenic Pithomyces strain.
New Zealand Veterinary Journal, 1995Co-Authors: R. G. Collin, N. R. TowersAbstract:Sporidesmin, a mycotoxin produced by some strains of Pithomyces chartarum, is responsible for the hepatogenous photosensitisation disease Facial Eczema, which causes severe losses in agricultural revenue in New Zealand. A sporidesmin-producing strain of P. chartarum, isolated in New Zealand, was grown in co-culture with a South African strain that does not produce the mycotoxin. Competition occurred between the two strains when grown both on agar plates and on dried ryegrass, with a significant decrease in the total amount of sporidesmin produced. Biological control of toxigenic P. chartarum can thus occur under laboratory conditions, raising the possibility of similar control in the field situation.
