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Coassin, S.

Publications and source records attributed to Coassin, S..

4 recordsLinked to original sources

Nanopore sequencing with unique molecular identifiers enables accurate mutation analysis and haplotyping in the complex Lipoprotein(a) KIV-2 VNTR

BackgroundRepetitive genome regions, such as variable number of tandem repeats (VNTR) or short tandem repeats (STR), are major constituents of the uncharted dark genome and evade conventional sequencing approaches. The protein-coding LPA kringle IV type-2 (KIV-2) VNTR (5.6 kb per unit, 1-40 units per allele) is a medically highly relevant example with a particularly intricate structure, multiple haplotypes, intragenic homologies and an intra-VNTR STR. It is the primary regulator of plasma lipoprotein(a) [Lp(a)] concentrations, an important cardiovascular risk factor. However, despite Lp(a) variance is mostly genetically determined, Lp(a) concentrations vary widely between individuals and ancestries. This VNTR region hides multiple causal variants and functional haplotypes. MethodsWe evaluated the performance of amplicon-based nanopore sequencing with unique molecular identifiers (UMI-ONT-Seq) for SNP detection, haplotype mapping, VNTR unit consensus sequence generation and copy number estimation via coverage-corrected haplotypes quantification in the KIV-2 VNTR. We used 15 human samples and low-level mixtures (0.5% to 5%) of KIV-2 plasmids as a validation set. We then applied UMI-ONT-Seq to extract KIV-2 VNTR haplotypes in 48 multi-ancestry 1000-Genome samples and analyzed at scale a poorly characterized STR within the KIV-2 VNTR. ResultsUMI-ONT-Seq detected KIV-2 SNPs down to 1% variant level with high sensitivity, specificity and precision (0.977{+/-}0.018; 1.000{+/-}0.0005; 0.993{+/-}0.02) and accurately retrieved the full-length haplotype of each VNTR unit. Human variant levels were highly correlated with next-generation sequencing (R2=0.983) without bias across the whole variant level range. Six reads per UMI produced sequences of each KIV-2 unit with Q40-quality. The KIV-2 repeat number determined by coverage-corrected unique haplotype counting was in close agreement with droplet digital PCR (ddPCR), with 70% of the samples falling even within the narrow confidence interval of ddPCR. We then analyzed 62,679 intra-KIV-2 STR sequences and identified ancestry-specific STR patterns. Finally, we characterized the KIV-2 haplotype patterns across multiple ancestries. ConclusionsUMI-ONT-Seq accurately retrieves the SNP haplotype and precisely quantifies the VNTR copy number of each repeat unit of the complex KIV-2 VNTR region across multiple ancestries. This study utilizes the KIV-2 VNTR, presenting a novel and potent tool for comprehensive characterization of medically relevant complex genome regions at scale.

genomics↗

Investigation of an LPA KIV-2 nonsense mutation in 11,000 individuals: the importance of linkage disequilibrium structure in LPA genetics.

ObjectiveElevated Lp(a) plasma concentrations are determined mainly genetically by the LPA gene locus, but up to 70% of the coding sequence is located in the so-called "kringle IV type 2" (KIV-2) copy number variation. This region is not resolved by common genotyping technologies and large epidemiological studies on this region are therefore missing. The Arg21Ter variant (R21X, variant frequency {approx}2%) is a functional variant in this region, but it has never been analyzed in large cohorts and is it unknown whether it is captured by genome-wide association studies. Approach and ResultsWe developed a highly sensitive allele-specific qPCR assay and genotyped R21X in 10,910 individuals from three populations (GCKD, KORA F3, KORA F4). R21X carriers showed significantly lower mean Lp(a) concentrations (-11.7 mg/dL [-15.5;-7.82], p=3.39e-32). Of particular note, virtually all R21X carriers also carried the splice mutation rs41272114 (D=0.957, R2=0.275), as confirmed by pulsed-field gel electrophoresis and long-range haplotyping. This proposes that the R21X mutation arose on the background of the rs41272114 splice variant. ConclusionsWe performed the largest epidemiological study on an LPA KIV-2 variant so far. Interestingly, R21X is located on the same haplotype as the splice mutation rs41272114, creating "double-null" LPA alleles that are inactivated by two independent mutations. The effect of the R21X nonsense mutation can thus not be discerned from the effect of rs41272114 splice site mutation. This emphasizes the importance of assessing the complex LD structure within LPA even for functional variants.

genetics↗

A genome-wide analysis of DNA methylation identifies a novel association signal for Lp(a) concentrations in the LPA promoter

Lipoprotein(a) [Lp(a)] is a major cardiovascular risk factor, which is largely genetically determined by one major gene locus, the LPA gene. Many aspects of the transcriptional regulation of LPA are poorly understood and the role of epigenetics has not been addressed yet. Therefore, we conducted an epigenome-wide analysis of DNA methylation on Lp(a) levels in two population-based studies (total n=2208). We identified a CpG site in the LPA promoter which was significantly associated with Lp(a) concentrations. Surprisingly, the identified CpG site was found to overlap the SNP rs76735376. We genotyped this SNP de-novo in three studies (total n=7512). The minor allele of rs76735376 (1.1% minor allele frequency) was associated with increased Lp(a) values (p=1.01e-59) and explained 3.5% of the variation of Lp(a). Statistical mediation analysis showed that the effect on Lp(a) is rather originating from the base change itself and is not mediated by DNA methylation levels. This finding is supported by eQTL data from 153 liver tissue samples from the GTEx project, which shows a significant association of the rs76735376 minor allele with increased LPA expression. In summary, our data supports a functional role of rs76735376 in the regulation of LPA expression.

genetics↗

Cis-epistasis at the LPA locus and risk of coronary artery disease

Identification of epistasis affecting complex human traits has been challenging. Focusing on known coronary artery disease (CAD) risk loci, we explore pairwise statistical interactions between 8,068 SNPs from ten CAD genome-wide association studies (n=30,180). We discovered rs1800769 and rs9458001 in the vicinity of the LPA locus to interact in modulating CAD risk (P=1.75x10-13). Specific genotypes (e.g., rs1800769 CT) displayed either significantly decreased or increased risk for CAD in the context of genotypes of the respective other SNP (e.g., rs9458001 GG vs. AA). In the UK Biobank (n=450,112) significant interaction of this SNP pair was replicated for CAD (P=3.09x10-22), and was also found for aortic valve stenosis (P=6.95x10-7) and peripheral arterial disease (P=2.32x10-4). Identical interaction patterns affected circulating lipoprotein(a) (n=5,953; P=8.7x10-32) and hepatic apolipoprotein(a) (apo(a)) expression (n=522, P=2.6x10-11). We further interrogated potential biological implications of the variants and propose a mechanism explaining epistasis that ultimately may translate to substantial cardiovascular risks.

genetics↗