ArticleNature communications2020
SAMMY-seq reveals early alteration of heterochromatin and deregulation of bivalent genes in Hutchinson-Gilford Progeria Syndrome.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 51 citations in OpenAlex.
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- BMI1 represses G-quadruplex DNA formation to maintain genomic stability during replication.The Journal of biological chemistry · 2026Article
- Chromatin remodeling restrains oncogenic functions in prostate cancer.Nature communications · 2025Article
- The molecular basis of lamin-specific chromatin interactions.Nature structural & molecular biology · 2025Article
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- IT-scC&T-seq streamlines scalable, parallel profiling of protein-DNA interactions in single cells.Genome biology · 2025Article
- The genome in space and time comes of age.Nucleus (Austin, Tex.) · 2024Article
- Disorganized chromatin hierarchy and stem cell aging in a male patient of atypical laminopathy-based progeria mandibuloacral dysplasia type A.Nature communications · 2024Article
- Biochemical properties of chromatin domains define genome compartmentalization.Nucleic acids research · 2024Article
- Pediatric glioma histone H3.3 K27M/G34R mutations drive abnormalities in PML nuclear bodies.Genome biology · 2023Article
- MATR3-antisense LINE1 RNA meshwork scaffolds higher-order chromatin organization.EMBO reports · 2023Article
- Tissue fluidification promotes a cGAS-STING cytosolic DNA response in invasive breast cancer.Nature materials · 2023Article
- 2023 Padua Days of Muscle and Mobility Medicine: post-meeting Book of Abstracts.European journal of translational myology · 2023Article
- The Molecular and Cellular Basis of Hutchinson-Gilford Progeria Syndrome and Potential Treatments.Genes · 2023Review
- Abstracts of the 2023 Padua Days of Muscle and Mobility Medicine (2023Pdm3) to be held March 29 - April 1 at the Galileian Academy of Padua and at the Petrarca Hotel, Thermae of Euganean Hills, Padua, Italy.European journal of translational myology · 2023Article
- Measuring Inaccessible Chromatin Genome-Wide Using Protect-seq.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Polycomb Bodies Detection in Murine Fibromuscular Stroma from Skin, Skeletal Muscles, and Aortic Tissues.Methods in molecular biology (Clifton, N.J.) · 2023Article
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Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hutchinson-Gilford progeria syndrome is a genetic disease caused by an aberrant form of Lamin A resulting in chromatin structure disruption, in particular by interfering with lamina associated domains. Early molecular alterations involved in chromatin remodeling have not been identified thus far. Here, we present SAMMY-seq, a high-throughput sequencing-based method for genome-wide characterization of heterochromatin dynamics. Using SAMMY-seq, we detect early stage alterations of heterochromatin structure in progeria primary fibroblasts. These structural changes do not disrupt the distribution of H3K9me3 in early passage cells, thus suggesting that chromatin rearrangements precede H3K9me3 alterations described at later passages. On the other hand, we observe an interplay between changes in chromatin accessibility and Polycomb regulation, with site-specific H3K27me3 variations and transcriptional dysregulation of bivalent genes. We conclude that the correct assembly of lamina associated domains is functionally connected to the Polycomb repression and rapidly lost in early molecular events of progeria pathogenesis.
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