PDF(Pubmed)
Abstract：
BACKGROUND: Ovine footrot caused by Dichelobacter nodosus (D. nodosus) is a contagious disease with serious economic and welfare impacts in sheep production systems worldwide. A better understanding of the host genetic architecture regarding footrot resistance/susceptibility is crucial to develop disease control strategies that efficiently reduce infection and its severity. A genome-wide association study was performed using a customized SNP array (47,779 SNPs in total) to identify genetic variants associated to footrot resistance/susceptibility in two Portuguese native breeds, i.e. Merino Branco and Merino Preto, and a population of crossbred animals. A cohort of 1375 sheep sampled across 17 flocks, located in the Alentejo region (southern Portugal), was included in the analyses.
RESULTS: Phenotypes were scored from 0 (healthy) to 5 (severe footrot) based on visual inspection of feet lesions, following the Modified Egerton System. Using a linear mixed model approach, three SNPs located on chromosome 24 reached genome-wide significance after a Bonferroni correction (p < 0.05). Additionally, six genome-wide suggestive SNPs were identified each on chromosomes 2, 4, 7, 8, 9 and 15. The annotation and KEGG pathway analyses showed that these SNPs are located within regions of candidate genes such as the nonsense mediated mRNA decay associated PI3K related kinase (SMG1) (chromosome 24) and the RALY RNA binding protein like (RALYL) (chromosome 9), both involved in immunity, and the heparan sulfate proteoglycan 2 (HSPG2) (chromosome 2) and the Thrombospodin 1 (THBS1) (chromosome 7) implicated in tissue repair and wound healing processes.
CONCLUSIONS: This is the first attempt to identify molecular markers associated with footrot in Portuguese Merino sheep. These findings provide relevant information on a likely genetic association underlying footrot resistance/susceptibility and the potential candidate genes affecting this trait. Genetic selection strategies assisted on the information obtained from this study could enhance Merino sheep-breeding programs, in combination with farm management strategies, for a more effective and sustainable long-term solution for footrot control.
RESULTS: Phenotypes were scored from 0 (healthy) to 5 (severe footrot) based on visual inspection of feet lesions, following the Modified Egerton System. Using a linear mixed model approach, three SNPs located on chromosome 24 reached genome-wide significance after a Bonferroni correction (p < 0.05). Additionally, six genome-wide suggestive SNPs were identified each on chromosomes 2, 4, 7, 8, 9 and 15. The annotation and KEGG pathway analyses showed that these SNPs are located within regions of candidate genes such as the nonsense mediated mRNA decay associated PI3K related kinase (SMG1) (chromosome 24) and the RALY RNA binding protein like (RALYL) (chromosome 9), both involved in immunity, and the heparan sulfate proteoglycan 2 (HSPG2) (chromosome 2) and the Thrombospodin 1 (THBS1) (chromosome 7) implicated in tissue repair and wound healing processes.
CONCLUSIONS: This is the first attempt to identify molecular markers associated with footrot in Portuguese Merino sheep. These findings provide relevant information on a likely genetic association underlying footrot resistance/susceptibility and the potential candidate genes affecting this trait. Genetic selection strategies assisted on the information obtained from this study could enhance Merino sheep-breeding programs, in combination with farm management strategies, for a more effective and sustainable long-term solution for footrot control.
摘要：
背景：由结节性二重杆菌引起的绵羊脚病（D.nodosus）是一种传染性疾病，对全世界的绵羊生产系统具有严重的经济和福利影响。更好地了解有关脚腐病抗性/易感性的宿主遗传结构对于制定有效减少感染及其严重程度的疾病控制策略至关重要。使用定制的SNP阵列（总共47,779个SNP）进行了全基因组关联研究，以鉴定与两个葡萄牙本地品种的脚病抗性/易感性相关的遗传变异，即MerinoBranco和MerinoPreto,和一群杂交动物。一群1375只绵羊在17个羊群中取样，位于阿连特霍地区（葡萄牙南部），包括在分析中。
结果：根据足部病变的目视检查，将表型从0（健康）评分到5（严重的脚病）评分，遵循修改后的Egerton系统。使用线性混合模型方法，在Bonferroni校正后，位于24号染色体上的三个SNP达到了全基因组意义（p<0.05）。此外,在2,4,7,8,9和15号染色体上鉴定出6个全基因组暗示性SNP.注释和KEGG通路分析表明，这些SNP位于候选基因的区域内，例如无义介导的mRNA衰变相关的PI3K相关激酶（SMG1）（染色体24）和RALYRNA结合蛋白（RALYL）（染色体9），都参与了豁免权,硫酸乙酰肝素蛋白聚糖2（HSPG2）（2号染色体）和血栓形成蛋白1（THBS1）（7号染色体）参与组织修复和伤口愈合过程。
结论：这是首次尝试鉴定与葡萄牙美利奴羊的脚病相关的分子标记。这些发现提供了有关可能的遗传关联的相关信息，这些遗传关联可能是脚腐病抗性/易感性以及影响该性状的潜在候选基因。从这项研究中获得的信息辅助的遗传选择策略可以增强Merino绵羊育种计划，结合农场管理战略，为更有效和可持续的长期解决方案控制脚。
结果：根据足部病变的目视检查，将表型从0（健康）评分到5（严重的脚病）评分，遵循修改后的Egerton系统。使用线性混合模型方法，在Bonferroni校正后，位于24号染色体上的三个SNP达到了全基因组意义（p<0.05）。此外,在2,4,7,8,9和15号染色体上鉴定出6个全基因组暗示性SNP.注释和KEGG通路分析表明，这些SNP位于候选基因的区域内，例如无义介导的mRNA衰变相关的PI3K相关激酶（SMG1）（染色体24）和RALYRNA结合蛋白（RALYL）（染色体9），都参与了豁免权,硫酸乙酰肝素蛋白聚糖2（HSPG2）（2号染色体）和血栓形成蛋白1（THBS1）（7号染色体）参与组织修复和伤口愈合过程。
结论：这是首次尝试鉴定与葡萄牙美利奴羊的脚病相关的分子标记。这些发现提供了有关可能的遗传关联的相关信息，这些遗传关联可能是脚腐病抗性/易感性以及影响该性状的潜在候选基因。从这项研究中获得的信息辅助的遗传选择策略可以增强Merino绵羊育种计划，结合农场管理战略，为更有效和可持续的长期解决方案控制脚。
