ArticleNucleic acids research2009
DNaseI hypersensitivity at gene-poor, FSH dystrophy-linked 4q35.2.
Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- The myoblast methylome: multiple types of associations with chromatin and transcription.Epigenetics · 2025Article
- Diversity challenges and reconciles genetics in facioscapulohumeral muscular dystrophy.Journal of human genetics · 2025Review
- Scanning window analysis of non-coding regions within normal-tumor whole-genome sequence samples.Briefings in bioinformatics · 2021Article
- ZNF555 protein binds to transcriptional activator site of 4qA allele and ANT1: potential implication in Facioscapulohumeral dystrophy.Nucleic acids research · 2015Article
- DUX4 promotes transcription of FRG2 by directly activating its promoter in facioscapulohumeral muscular dystrophy.Skeletal muscle · 2014Article
- Deregulation of the protocadherin gene FAT1 alters muscle shapes: implications for the pathogenesis of facioscapulohumeral dystrophy.PLoS genetics · 2013Article
- Facioscapulohumeral muscular dystrophy: consequences of chromatin relaxation.Current opinion in neurology · 2012Review
- Deciphering transcription dysregulation in FSH muscular dystrophy.Journal of human genetics · 2012Review
- Gene expression during normal and FSHD myogenesis.BMC medical genomics · 2011Article
- DNA replication timing is maintained genome-wide in primary human myoblasts independent of D4Z4 contraction in FSH muscular dystrophy.PloS one · 2011Article
- Current concepts of follicle-stimulating hormone receptor gene regulation.Biology of reproduction · 2011Review
- FSH dystrophy and a subtelomeric 4q haplotype: a new assay and associations with disease.Journal of medical genetics · 2010Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
A subtelomeric region, 4q35.2, is implicated in facioscapulohumeral muscular dystrophy (FSHD), a dominant disease thought to involve local pathogenic changes in chromatin. FSHD patients have too few copies of a tandem 3.3-kb repeat (D4Z4) at 4q35.2. No phenotype is associated with having few copies of an almost identical repeat at 10q26.3. Standard expression analyses have not given definitive answers as to the genes involved. To investigate the pathogenic effects of short D4Z4 arrays on gene expression in the very gene-poor 4q35.2 and to find chromatin landmarks there for transcription control, unannotated genes and chromatin structure, we mapped DNaseI-hypersensitive (DH) sites in FSHD and control myoblasts. Using custom tiling arrays (DNase-chip), we found unexpectedly many DH sites in the two large gene deserts in this 4-Mb region. One site was seen preferentially in FSHD myoblasts. Several others were mapped >0.7 Mb from genes known to be active in the muscle lineage and were also observed in cultured fibroblasts, but not in lymphoid, myeloid or hepatic cells. Their selective occurrence in cells derived from mesoderm suggests functionality. Our findings indicate that the gene desert regions of 4q35.2 may have functional significance, possibly also to FSHD, despite their paucity of known genes.
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Registered trials
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