Marini Nicholas J, Yang Wei, Asrani Kripa, Witte John S, Rine Jasper, Lammer Edward J, Shaw Gary M
Department of Molecular and Cellular Biology, California Institute for Quantitative Biosciences, University of California, Berkeley, California.
Department of Pediatrics, Stanford University School of Medicine, Stanford, California.
Am J Med Genet A. 2016 Nov;170(11):2777-2787. doi: 10.1002/ajmg.a.37874. Epub 2016 Sep 8.
In an effort to comprehensively interrogate genetic variation in the folate pathway for risk of cleft lip with or without cleft palate (CLP), we evaluated 504 common and rare variants in 35 folate-related genes in a panel of 330 infants with CLP and 367 non-malformed controls. Odds ratios (OR) with 95% confidence intervals were computed for common genotypes. A Case-Control Difference metric was calculated for rare variants to highlight differentially occurring alleles. Interactions between variants and a maternal folate intake variable were also evaluated. In gene-only results, significant odds ratios were observed for multiple variants in the BHMT/BHMT2/DMGDH gene cluster, particularly in Hispanic infants. Also in this cluster, rare variant analysis highlighted a substantial case-control difference in BHMT rs60340837 (synonymous Y284Y). In Hispanics, the ALDH1L1 I812V variant (rs4646750) was the most significant risk allele: OR = 3.8 (95%CI = 1.6-9.2) when heterozygous. In non-Hispanic white infants, we observed significant risk for AHCYL2 rs1095423 (homozygous OR = 3.0, 95%CI 1.1-7.8) and the 68 bp CBS insertion (c.844ins68; heterozygous OR = 2.4, 95%CI = 1.1-5.3). Rare variant analysis in this group revealed case-control differences in MTRR and several other methionine cycle genes, a process implicated previously in clefting risk. In women with low folate intake specifically, increased risks were observed for CBS rs2851391 (OR = 3.6, 95%CI = 1.3-9.6) and the R259P nonsynonymous variant of TCN2 (rs1801198; OR = 2.8, 95%CI = 1.2-6.3). This comprehensive study provides further direction on candidate loci to help disentangle the folate-related developmental phenomena in human clefting risk. © 2016 Wiley Periodicals, Inc.
为了全面探究叶酸代谢途径中的基因变异与唇裂伴或不伴腭裂(CLP)风险之间的关系,我们在330例CLP婴儿和367例非畸形对照组成的样本中,评估了35个叶酸相关基因中的504个常见和罕见变异。计算了常见基因型的优势比(OR)及其95%置信区间。针对罕见变异计算了病例对照差异指标,以突出差异出现的等位基因。还评估了变异与母亲叶酸摄入量变量之间的相互作用。仅在基因层面的结果中,在BHMT/BHMT2/DMGDH基因簇中的多个变异观察到显著的优势比,特别是在西班牙裔婴儿中。同样在这个基因簇中,罕见变异分析突出了BHMT基因rs60340837(同义突变Y284Y)在病例组和对照组之间存在显著差异。在西班牙裔人群中,ALDH1L1基因的I812V变异(rs4646750)是最显著的风险等位基因:杂合时OR = 3.8(95%CI = 1.6 - 9.2)。在非西班牙裔白人婴儿中,我们观察到AHCYL2基因rs1095423存在显著风险(纯合时OR = 3.0,95%CI 1.1 - 7.8)以及CBS基因68bp插入突变(c.844ins68;杂合时OR = 2.4,95%CI = 1.1 - 5.3)。该组的罕见变异分析显示,MTRR基因和其他几个甲硫氨酸循环基因在病例组和对照组之间存在差异,此前有研究表明该过程与腭裂风险有关。特别是在叶酸摄入量低的女性中,观察到CBS基因rs2851391(OR = 3.6,95%CI = 1.3 - 9.6)和TCN2基因的R259P非同义变异(rs1801198;OR = 2.8,95%CI = 1.2 - 6.3)的风险增加。这项综合性研究为候选基因座提供了进一步的方向,以帮助理清与叶酸相关的人类腭裂风险发育现象。© 2016威利期刊公司