Experimental designs that exploit family information can provide substantial predictive power in quantitative trait nucleotide discovery projects. Concordance between quantitative trait locus genotype as determined by the a posteriori granddaughter design and marker genotype was determined for 30 trait-by-chromosomal segment effects segregating in the US Holstein population with probabilities of <10⁻²⁰ to accept the null hypotheses of no segregating gene affecting the trait within the chromosomal segment. Genotypes for 83 grandsires and 17,217 sons were determined by either complete sequence or imputation for 3,148,506 polymorphisms across the entire genome; 471 Holstein bulls had a complete genome sequence, including 64 of the grandsires. Complete concordance was obtained only for stature on chromosome 14 and daughter pregnancy rate on chromosome 18. For each quantitative trait locus, effects of the 30 polymorphisms with highest concordance scores for the analyzed trait were computed by stepwise regression for predicted transmitting abilities of 26,750 bulls with progeny test and imputed genotypes. Effects for stature on chromosome 11, daughter pregnancy rate on chromosome 18, and protein percentage on chromosome 20 met 3 criteria: complete or almost complete concordance, nominal significance of the polymorphism effect after correction for all other polymorphisms, and marker coefficient of determination >40% of total multiple-regression coefficient of determination for the 30 polymorphisms with highest concordance. An intronic variant marker on chromosome 5 at 93,945,738 bp explained 7% of variance for fat percentage and 74% of total multiple-marker regression variance but was concordant for only 24 of 30 families. The missense polymorphism Phe279Tyr in GHR at 31,909,478 bp on chromosome 20 was confirmed as the causative mutation for fat and protein concentration. For effect on fat percentage on chromosome 14, 12 additional missense polymorphisms were found that had almost complete concordance with the suggested causative polymorphism (missense mutation Ala232Glu in DGAT1). The only polymorphism found likely to improve predictive power for genomic evaluation of dairy cattle was on chromosome 15; that polymorphism had a frequency of 0.45 for the allele with economically positive effects on all production traits.

利用家族信息的实验设计可以在定量性状核苷酸发现项目中提供重要的预测能力。通过后代孙女设计确定的数量性状基因座基因型与标记基因型之间的一致性，针对美国荷斯坦州人群中30种按特征分类的染色体区段效应进行了确定，概率＜10 ^-20接受没有分离基因影响染色体片段内性状的无效假设。通过对整个基因组的3,148,506个多态性进行完整序列分析或插补，确定了83个孙代和17,217个子代的基因型。471头荷斯坦公牛具有完整的基因组序列，其中包括64个孙代。仅在14号染色体上的身高和18号染色体上的子代怀孕率获得完全一致性。对于每个定量性状基因座，通过逐步回归计算预测的26,750头公牛的传播能力，计算出30个具有最高一致性得分的被分析性状的效应。后代测试和估算的基因型。身材对11号染色体的影响，18号染色体的女儿怀孕率和20号染色体的蛋白质百分比均符合以下三个标准：完全一致或几乎完全一致，对所有其他多态性进行校正后，多态性效应的名义显着性，对于最高一致性的30个多态性，确定的标记系数大于确定的总多次回归系数的40％。5号染色体上的内含子变异标记为93,945,738 bp，解释了脂肪百分比的变异7％和总多标记回归变异的74％，但在30个家庭中只有24个是一致的。中的错义多态性Phe279Tyr 5号染色体上的内含子变异标记为93,945,738 bp，解释了脂肪百分比的变异7％和总多标记回归变异的74％，但在30个家庭中只有24个是一致的。中的错义多态性Phe279Tyr 5号染色体上的内含子变异标记为93,945,738 bp，解释了脂肪百分比的变异7％和总多标记回归变异的74％，但在30个家庭中只有24个是一致的。中的错义多态性Phe279Tyr在20号染色体上的31,909,478 bp处的GHR被确认为脂肪和蛋白质浓度的致病突变。有关14号染色体上的脂肪比例的效果，增加12个错义多态性发现，用建议的致病多态性（错义突变Ala232Glu在几乎完全一致DGAT1）。发现唯一可能改善奶牛基因组评估预测能力的多态性位于第15号染色体上。该等位基因的多态性频率为0.45，对所有生产性状均具有经济上的积极影响。