ArticleMolecular and cellular biology2013
Cdyl, a new partner of the inactive X chromosome and potential reader of H3K27me3 and H3K9me2.
Article in Molecular and cellular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- From inactivation to intervention: X chromosome silencing in disease pathogenesis and emerging therapeutic strategies.Genes & diseases · 2026Review
- Structural landscape of H3K27me3 recognition by protein domains and their potential for inhibition.The Journal of biological chemistry · 2026Review
- Chromatin-Based Control of Mammalian Sex Determination: Integrating Epigenetic and Metabolic Mechanisms.Advances in experimental medicine and biology · 2026Review
- CDYL reinforces male gonadal sex determination through epigenetically repressingProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Establishment of H3K9-methylated heterochromatin and its functions in tissue differentiation and maintenance.Nature reviews. Molecular cell biology · 2022Review
- STAT5A modulates CDYL2/SLC7A6 pathway to inhibit the proliferation and invasion of hepatocellular carcinoma by targeting to mTORC1.Oncogene · 2022Article
- Gene regulation in time and space during X-chromosome inactivation.Nature reviews. Molecular cell biology · 2022Review
- Cdyl Deficiency Brakes Neuronal Excitability and Nociception through Promoting Kcnb1 Transcription in Peripheral Sensory Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- The control of polycomb repressive complexes by long noncoding RNAs.Wiley interdisciplinary reviews. RNA · 2021Review
- A disproportionate impact of G9a methyltransferase deficiency on the X chromosome.Genes & development · 2021Article
- Mapping the micro-proteome of the nuclear lamina and lamina-associated domains.Life science alliance · 2021Article
- Small Molecules Targeting the Specific Domains of Histone-Mark Readers in Cancer Therapy.Molecules (Basel, Switzerland) · 2020Review
- Article
- A Degenerate Peptide Library Approach to Reveal Sequence Determinants of Methyllysine-Driven Protein Interactions.Frontiers in cell and developmental biology · 2020Article
- Loss of CDYL Results in Suppression of CTNNB1 and Decreased Endometrial Receptivity.Frontiers in cell and developmental biology · 2020Article
- Germline deletion of Cdyl causes teratozoospermia and progressive infertility in male mice.Cell death & disease · 2019Article
- Investigation of the Developmental Requirements of Drosophila HP1 and Insulator Protein Partner, HIPP1.G3 (Bethesda, Md.) · 2019Article
- The Role of RNA Polymerase II Contiguity and Long-Range Interactions in the Regulation of Gene Expression in Human Pluripotent Stem Cells.Stem cells international · 2019Article
- CDYL promotes the chemoresistance of small cell lung cancer by regulating H3K27 trimethylation at the CDKN1C promoter.Theranostics · 2019Article
- Polycomb protein family member CBX7 regulates intrinsic axon growth and regeneration.Cell death and differentiation · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
X chromosome inactivation is a remarkable example of chromosome-wide gene silencing and facultative heterochromatin formation. Numerous histone posttranslational modifications, including H3K9me2 and H3K27me3, accompany this process, although our understanding of the enzymes that lay down these marks and the factors that bind to them is still incomplete. Here we identify Cdyl, a chromodomain-containing transcriptional corepressor, as a new chromatin-associated protein partner of the inactive X chromosome (Xi). Using mouse embryonic stem cell lines with mutated histone methyltransferase activities, we show that Cdyl relies on H3K9me2 for its general association with chromatin in vivo. For its association with Xi, Cdyl requires the process of differentiation and the presence of H3K9me2 and H3K27me3, which both become chromosomally enriched following Xist RNA coating. We further show that the removal of the PRC2 component Eed and subsequent loss of H3K27me3 lead to a reduction of both Cdyl and H3K9me2 enrichment on inactive Xi. Finally, we show that Cdyl associates with the H3K9 histone methyltransferase G9a and the MGA protein, both of which are also found on Xi. We propose that the combination of H3K9me2 and H3K27me3 recruits Cdyl to Xi, and this, in turn, may facilitate propagation of the H3K9me2 mark by anchoring G9a.
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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.