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Background: Understanding the genetic contribution to phenotype variation of human groups is necessary to elucidate differences in disease predisposition and response to pharmaceutical treatments in different human populations.
Methodology/principal Findings: We have investigated the genome-wide profile of structural variation on pooled samples from the three populations studied in the HapMap project by comparative genome hybridization (CGH) in different array platforms. We have identified and experimentally validated 33 genomic loci that show significant copy number differences from one population to the other. Interestingly, we found an enrichment of genes related to environment adaptation (immune response, lipid metabolism and extracellular space) within these regions and the study of expression data revealed that more than half of the copy number variants (CNVs) translate into gene-expression differences among populations, suggesting that they could have functional consequences. In addition, the identification of single nucleotide polymorphisms (SNPs) that are in linkage disequilibrium with the copy number alleles allowed us to detect evidences of population differentiation and recent selection at the nucleotide variation level.
Conclusions: Overall, our results provide a comprehensive view of relevant copy number changes that might play a role in phenotypic differences among major human populations, and generate a list of interesting candidates for future studies.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2747275 | PMC |
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0007230 | PLOS |
Front Endocrinol (Lausanne)
December 2024
Medical Research Institute KITANO HOSPITAL, PIIF Tazuke-kofukai, Osaka, Japan.
Silver-Russell syndrome (SRS) is a syndrome characterized by prenatal and postnatal growth retardation, facial features, and body asymmetry. SRS is often complicated with hypoglycemia, whose etiology is unclear. We describe the clinical course of 25-year-old man with hypoglycemia.
View Article and Find Full Text PDFBMC Bioinformatics
December 2024
Albert Szent-Györgyi Health Centre, University of Szeged, Korányi fasor 14-15, Szeged, H-6725, Csongrád-Csanád, Hungary.
Background: Accurate prediction of copy number variations (CNVs) from targeted capture next-generation sequencing (NGS) data relies on effective normalization of read coverage profiles. The normalization process is particularly challenging due to hidden systemic biases such as GC bias, which can significantly affect the sensitivity and specificity of CNV detection. In many cases, the kit manifests provide only the genome coordinates of the targeted regions, and the exact bait design of the oligo capture baits is not available.
View Article and Find Full Text PDFEye (Lond)
December 2024
Singapore Eye Research Institute, Singapore National Eye Centre, Singapore, Singapore.
Objectives: To determine the association between telomere length (TL) and age-related macular degeneration (AMD) and examine the potential variations with sex and ethnicity.
Methods: Population-based, cross-sectional study. A total of 52,083 participants from the UK Biobank were included.
Orphanet J Rare Dis
December 2024
The Center for Pediatric Liver Diseases, Children's Hospital of Fudan University, 399 Wanyuan Road, Minhang District, Shanghai, 201102, China.
Mitochondrial transcription factor A (TFAM) deficiency may cause mtDNA depletion syndrome, which manifests as neonatal liver failure or primary ovarian insufficiency, hearing loss, seizures, and intellectual disability. Treatment focusing on symptomatic management, and the clinical prognosis remains poor. Here, we describe a novel case of TFAM mutation presenting with progressive neonatal cholestasis, hypoglycemia and abnormal amino acid profiling.
View Article and Find Full Text PDFBMC Med Genomics
December 2024
Department of Pediatrics, Sichuan Provincial Woman's and Children's Hospital, The Affiliated Women's and Children's Hospital of Chengdu Medical College, Chengdu, China.
Background: Pure partial trisomy 16q12.1q22.1 is a rare chromosome copy number variant (CNV).
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