Meng Haijin, Vera Iset, Che Nam, Wang Xuping, Wang Susanna S, Ingram-Drake Leslie, Schadt Eric E, Drake Thomas A, Lusis Aldons J
Department of Medicine, Cardiology Division, University of California-Los Angeles, Los Angeles, CA 90095, USA.
Proc Natl Acad Sci U S A. 2007 Mar 13;104(11):4530-5. doi: 10.1073/pnas.0607620104. Epub 2007 Mar 6.
The genetic factors contributing to the complex disorder of myocardial calcification are largely unknown. Using a mouse model, we fine-mapped the major locus (Dyscalc1) contributing to the dystrophic cardiac calcification (DCC) to an 840-kb interval containing 38 genes. We then identified the causal gene by using an approach integrating genetic segregation and expression array analyses to identify, on a global scale, cis-acting DNA variations that perturb gene expression. By studying two intercrosses, in which the DCC trait segregates, a single candidate gene (encoding the ATP-binding cassette transporter ABCC6) was identified. Transgenic complementation confirmed Abcc6 as the underlying causal gene for Dyscalc1. We demonstrate that in the cross, the expression of Abcc6 is highly correlated with the local mineralization regulatory system and the BMP2-Wnt signaling pathway known to be involved in the systemic regulation of calcification, suggesting potential pathways for the action of Abcc6 in DCC. Our results demonstrate the power of the integrative genomics in discovering causal genes and pathways underlying complex traits.
导致心肌钙化这种复杂病症的遗传因素在很大程度上尚不清楚。利用小鼠模型,我们将导致营养不良性心脏钙化(DCC)的主要基因座(Dyscalc1)精细定位到一个包含38个基因的840 kb区间。然后,我们通过整合遗传分离和表达阵列分析的方法来鉴定因果基因,以便在全球范围内识别干扰基因表达的顺式作用DNA变异。通过研究两个DCC性状发生分离的杂交组合,我们鉴定出了一个单一的候选基因(编码ATP结合盒转运蛋白ABCC6)。转基因互补实验证实Abcc6是Dyscalc1的潜在因果基因。我们证明,在杂交中,Abcc6的表达与局部矿化调节系统以及已知参与钙化全身调节的BMP2 - Wnt信号通路高度相关,这表明Abcc6在DCC中发挥作用的潜在途径。我们的结果证明了整合基因组学在发现复杂性状潜在因果基因和途径方面的强大作用。