1 Institute of Agricultural Sciences, ETH Zurich, 8092 Zurich, Switzerland.
2 Department of Farm Animals, Vetsuisse Faculty, University of Zurich, 8057 Zurich, Switzerland.
Animal. 2014 Jun;8(6):859-66. doi: 10.1017/S1751731114000779. Epub 2014 Apr 11.
Enteric Escherichia coli infections are a highly relevant cause of disease and death in young pigs. Breeding genetically resistant pigs is an economical and sustainable method of prevention. Resistant pigs are protected against colonization of the intestine through the absence of receptors for the bacterial fimbriae, which mediate adhesion to the intestinal surface. The present work aimed at elucidation of the mode of inheritance of the F4ad receptor which according to former investigations appeared quite confusing. Intestines of 489 pigs of an experimental herd were examined by a microscopic adhesion test modified in such a manner that four small intestinal sites instead of one were tested for adhesion of the fimbrial variant F4ad. Segregation analysis revealed that the mixed inheritance model explained our data best. The heritability of the F4ad phenotype was estimated to be 0.7±0.1. There are no relations to the strong receptors for variants F4ab and F4ac. Targeted matings allowed the discrimination between two F4ad receptors, that is, a fully adhesive receptor (F4adRFA) expressed on all enterocytes and at all small intestinal sites, and a partially adhesive receptor (F4adRPA) variably expressed at different sites and often leading to partial bacterial adhesion. In pigs with both F4ad receptors, the F4adRPA receptor is masked by the F4adRFA. The hypothesis that F4adRFA must be encoded by at least two complementary or epistatic dominant genes is supported by the Hardy-Weinberg equilibrium statistics. The F4adRPA receptor is inherited as a monogenetic dominant trait. A comparable partially adhesive receptor for variant F4ab (F4abRPA) was also observed but the limited data did not allow a prediction of the mode of inheritance. Pigs were therefore classified into one of eight receptor phenotypes: A1 (F4abRFA/F4acR+/F4adRFA); A2 (F4abRFA/F4acR+/F4adRPA); B (F4abRFA/F4acR+/F4adR-); C1 (F4abRPA/F4acR-/F4adRFA); C2 (F4abRPA/F4acR-/F4adRPA); D1 (F4abR-/F4acR-/F4adRFA); D2 (F4abR-/F4acR-/F4adRPA); E (F4abR-/F4acR-/F4adR-).
肠型大肠杆菌感染是小猪发病和死亡的一个重要原因。培育具有遗传抗性的猪是一种经济且可持续的预防方法。通过缺乏细菌菌毛的受体,猪可以防止肠道定植,菌毛介导与肠道表面的黏附。本工作旨在阐明 F4ad 受体的遗传模式,根据以前的研究,该受体似乎非常混乱。通过改良的显微镜黏附试验,检查了一个实验性猪群的 489 头猪的肠道,该试验检测了 4 个小肠部位而不是 1 个部位的菌毛变体 F4ad 的黏附。分离分析表明,混合遗传模型最能解释我们的数据。F4ad 表型的遗传力估计为 0.7±0.1。与变体 F4ab 和 F4ac 的强受体没有关系。靶向交配允许区分两种 F4ad 受体,即完全黏附受体(F4adRFA),在所有肠细胞和所有小肠部位表达,以及部分黏附受体(F4adRPA),在不同部位表达可变,常导致部分细菌黏附。在具有两种 F4ad 受体的猪中,F4adRPA 受体被 F4adRFA 掩盖。F4adRFA 必须由至少两个互补或上位显性基因编码的假设得到了 Hardy-Weinberg 平衡统计的支持。F4adRPA 受体是一种单基因显性遗传性状。还观察到了变体 F4ab 的类似部分黏附受体(F4abRPA),但有限的数据不允许预测遗传模式。因此,猪被分为 8 种受体表型之一:A1(F4abRFA/F4acR+/F4adRFA);A2(F4abRFA/F4acR+/F4adRPA);B(F4abRFA/F4acR+/F4adR-);C1(F4abRPA/F4acR-/F4adRFA);C2(F4abRPA/F4acR-/F4adRPA);D1(F4abR-/F4acR-/F4adRFA);D2(F4abR-/F4acR-/F4adRPA);E(F4abR-/F4acR-/F4adR-)。