ArticleEpigenetics2013
Holocarboxylase synthetase synergizes with methyl CpG binding protein 2 and DNA methyltransferase 1 in the transcriptional repression of long-terminal repeats.
Article in Epigenetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- MeCP2 functions as a DNA methylation reader in immune homeostasis and cancer.Frontiers in epigenetics and epigenomics · 2026Review
- Biotin attenuates heat shock factor 4b transcriptional activity by lysine 444 biotinylation.Biochemistry and biophysics reports · 2022Article
- Article
- Suv420 enrichment at the centromere limits Aurora B localization and function.Journal of cell science · 2021Article
- MeCP2: The Genetic Driver of Rett Syndrome Epigenetics.Frontiers in genetics · 2021Review
- Resveratrol compounds inhibit human holocarboxylase synthetase and cause a lean phenotype in Drosophila melanogaster.The Journal of nutritional biochemistry · 2015Article
- Rett syndrome: a complex disorder with simple roots.Nature reviews. Genetics · 2015Review
- Beyond protein expression, MOPED goes multi-omics.Nucleic acids research · 2015Article
- β-Keto and β-hydroxyphosphonate analogs of biotin-5'-AMP are inhibitors of holocarboxylase synthetase.Bioorganic & medicinal chemistry letters · 2014Article
- Holocarboxylase synthetase interacts physically with nuclear receptor co-repressor, histone deacetylase 1 and a novel splicing variant of histone deacetylase 1 to repress repeats.The Biochemical journal · 2014Article
- Nuclear receptors and epigenetic regulation: opportunities for nutritional targeting and disease prevention.Advances in nutrition (Bethesda, Md.) · 2014Review
- Novel roles of holocarboxylase synthetase in gene regulation and intermediary metabolism.Nutrition reviews · 2014Review
- Holocarboxylase synthetase catalyzes biotinylation of heat shock protein 72, thereby inducing RANTES expression in HEK-293 cells.American journal of physiology. Cell physiology · 2013Article
- Epigenetic synergies between biotin and folate in the regulation of pro-inflammatory cytokines and repeats.Scandinavian journal of immunology · 2013Article
- Health promoting effects of brassica-derived phytochemicals: from chemopreventive and anti-inflammatory activities to epigenetic regulation.Oxidative medicine and cellular longevity · 2013Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Holocarboxylase synthetase (HLCS) is a chromatin protein that facilitates the creation of histone H3 lysine 9-methylation (H3K9me) gene repression marks through physical interactions with the histone methyltransferase EHMT-1. HLCS knockdown causes a depletion of H3K9me marks in mammalian cell cultures and severe phenotypes such as short lifespan and low stress resistance in Drosophila melanogaster. HLCS displays a punctuate distribution pattern in chromatin despite lacking a strong DNA-binding domain. Previous studies suggest that the binding of HLCS to chromatin depends on DNA methylation. We tested the hypothesis that HLCS interacts physically with the DNA methyltransferase DNMT1 and the methyl CpG binding protein MeCP2 to facilitate the binding of HLCS to chromatin, and that these interactions contribute toward the repression of long-terminal repeats (LTRs) by H3K9me marks. Co-immunoprecipitation and limited proteolysis assays provided evidence suggesting that HLCS interacts physically with both DNMT1 and MeCP2. The abundance of H3K9me marks was 207% greater in the LTR15 locus in HLCS overexpression human embryonic kidney HEK293 cells compared with controls. This gain in H3K9me was inversely linked with a 87% decrease in mRNA coding for LTRs. Effects of HLCS abundance on LTR expression were abolished when DNA methylation marks were erased by treating cells with 5-azacytidine. We conclude that interactions between DNA methylation and HLCS are crucial for mediating gene repression by H3K9me, thereby providing evidence for epigenetic synergies between the protein biotin ligase HLCS and dietary methyl donors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.