Beygo Jasmin, Ammerpohl Ole, Gritzan Daniela, Heitmann Melanie, Rademacher Katrin, Richter Julia, Caliebe Almuth, Siebert Reiner, Horsthemke Bernhard, Buiting Karin
Institut für Humangenetik, Universitätsklinikum Essen, Universität Duisburg-Essen, Essen, Germany.
PLoS One. 2013 Oct 9;8(10):e76953. doi: 10.1371/journal.pone.0076953. eCollection 2013.
NLRP7 is a maternal effect gene as maternal mutations in this gene cause recurrent hydatidiform moles, spontaneous abortions and stillbirths, whereas live births are very rare. We have studied a patient with multiple anomalies born to a mother with a heterozygous NLRP7 mutation. By array-based CpG methylation analysis of blood DNA from the patient, his parents and 18 normal controls on Illumina Infinium HumanMethylation27 BeadChips we found that the patient had methylation changes (delta ß ≥ 0.3) at many imprinted loci as well as at 87 CpGs associated with 85 genes of unknown imprinting status. Using a pseudoproband (permutation) approach, we found methylation changes at only 7-24 CpGs (mean 15; standard deviation 4.84) in the controls. Thus, the number of abberantly methylated CpGs in the patient is more than 14 standard deviations higher. In order to identify novel imprinted genes among the 85 conspicuous genes in the patient, we selected 19 (mainly hypomethylated) genes for deep bisulfite amplicon sequencing on the ROCHE/454 Genome Sequencer in the patient and at least two additional controls. These controls had not been included in the array analysis and were heterozygous for a single nucleotide polymorphism at the test locus, so that allele-specific DNA methylation patterns could be determined. Apart from FAM50B, which we proved to be imprinted in blood, we did not observe allele-specific DNA methylation at the other 18 loci. We conclude that the patient does not only have methylation defects at imprinted loci but (at least in blood) also an excess of methylation changes at apparently non-imprinted loci.
NLRP7是一种母系效应基因,因为该基因的母系突变会导致复发性葡萄胎、自然流产和死产,而活产则非常罕见。我们研究了一名患有多种异常的患者,其母亲存在杂合的NLRP7突变。通过在Illumina Infinium HumanMethylation27 BeadChips上对患者、其父母及18名正常对照者的血液DNA进行基于芯片的CpG甲基化分析,我们发现该患者在许多印记位点以及与85个印记状态未知基因相关的87个CpG处存在甲基化变化(δβ≥0.3)。使用虚拟先证者(置换)方法,我们发现对照者中仅有7 - 24个CpG(平均15个;标准差4.84)存在甲基化变化。因此,患者中异常甲基化的CpG数量比对照者高出14个标准差以上。为了在患者的85个显著基因中鉴定新的印记基因,我们选择了19个(主要是低甲基化)基因,在患者及至少另外两名对照者中,利用罗氏/454基因组测序仪进行深度亚硫酸氢盐扩增子测序。这些对照者未纳入芯片分析,且在测试位点的单核苷酸多态性为杂合状态,因此可以确定等位基因特异性DNA甲基化模式。除了我们证明在血液中存在印记的FAM50B外,我们在其他18个位点未观察到等位基因特异性DNA甲基化。我们得出结论,该患者不仅在印记位点存在甲基化缺陷,而且(至少在血液中)在明显非印记位点也存在过多的甲基化变化。