Ask about this productRelated genes to: SUV39H2 Blocking Peptide
- Gene:
- SUV39H2 NIH gene
- Name:
- suppressor of variegation 3-9 homolog 2
- Previous symbol:
- -
- Synonyms:
- FLJ23414, KMT1B
- Chromosome:
- 10p13
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-11
- Date modifiied:
- 2015-12-04
Related products to: SUV39H2 Blocking Peptide
Related articles to: SUV39H2 Blocking Peptide
- Despite the expression of multiple transcript isoforms from a gene, conventional gene expression analyses assume that a single transcript is expressed from each gene. We analyzed the transcript isoforms expressed in gonadotropin-induced mouse mural and cumulus granulosa cells (mGCs and cGCs) isolated from antral follicles to elucidate the potential mechanism of differentiation. Considering that either a single transcript or multiple isoforms are expressed from genes, we identified differential expression of about 70% of transcripts between mGCs and cGCs. Although the differential expressions were similar, the single-transcript-wise differentially expressed genes did not correlate with their corresponding differentially expressed transcript isoforms. We identified transcript isoforms of key transcriptional regulators in ovaries, including Chd1, Ezh2, Kdm5a/5b, Gata4, Esr2, Fos, Myc, and Ybx1, that were not identified in single-transcript-based analyses. Further analysis revealed a transcript switch in more than 30% of the differentially expressed isoforms. While one or more transcript isoforms of Cebpa, Dnmt3a, Pgr, Rest, Runx1, and Sirt1 were switched off, those of Brd7, Chd1, Med21, Nfkbia, Rbm39, Suv39h2, Tcf12, Xist, and Ybx3 were switched on in cGCs. Interestingly, several genes, including Dab2, Ezh2, Gata4, Gnas, Gtf2i, Klf10, Setdb1, and Sp3, exhibited at least one isoform that was switched off and another that was switched on in cGCs. Transcript switching was primarily due to alternative splicing, followed by alternative transcription start sites and polyadenylation sites. We also identified differential expression of the potential regulators of such transcript switching in cGCs. Our results suggest that transcript switching may play an important role in mural and cumulus granulosa differentiation, a key insight that would remain unknown without mRNA isoform analysis. - Source: PubMed
Publication date: 2026/05/23
Shila SharminPei Grace JBahadursingh ElizabethPeramsetty NikiDahiya VineshMarsh Courtney AThiyagarajan RamkumarZhang MeijiaFields Patrick ERumi M A Karim - Liver and lymph node endothelial cell C-type lectin (LSECtin) loss in liver sinusoidal endothelial cells (LSECs) during cirrhosis favors hepatic pro-inflammatory T-cell infiltration. We characterize histone protein post-translational modifications and DNA methylation in LSECs that may control LSECtin expression and evaluate methyltransferase inhibitors' capacity to retrieve LSECtin. - Source: PubMed
Publication date: 2026/05/22
Ángel-Gomis EnriqueGómez-Hurtado IsabelFernández-Barrena Maite GJuanola OriolMartínez-López SebastiánBoix PaulaÁvila Matías ACaparrós EstherFrancés Rubén - Histone H3K9me3 silences repetitive elements and represses non-lineage genes during early development, but its role in organogenesis is understudied. Here, we show that H3K9me3 deposition is dynamic during epidermis morphogenesis and essential for lineage diversification. We ablate Suv39h1, Suv39h2, and Setdb1 histone methyltransferases, in the embryonic mouse epidermis, to induce H3K9me3 loss. This causes complete failure of keratinocyte differentiation, skin barrier formation, hair follicle development, and Merkel cell specification. Single-cell transcriptomics reveals aberrant cell fates with mixed epidermal subtype identities and dysregulated non-lineage and lineage-specific transcription programs. Affected pathways include differentiation, metabolism, cell cycle, cytoskeletal organization, and extracellular matrix. H3K9me3 primarily restricts RNA Pol II transcription initiation at key developmental promoters and enhancers and has minimal direct effect on promoter-proximal pause release. We uncover a cooperative and indispensable role for Suv39h1, Suv39h2, and Setdb1 in gene expression control of epidermal morphogenesis, establishing H3K9me3 as a critical developmental determinant of skin organogenesis. - Source: PubMed
Publication date: 2026/05/15
Bai Chris KeChovatiya GopalPollack Emily JanineLiao Yu-ChingKim Ashley NayeonTumbar Tudorita - Suv39h1 and Suv39h2 are core components of mouse heterochromatin, where they direct H3K9me3, which is recognized by HP1. In mouse embryonic fibroblasts, heterochromatin retention modes of Suv39h enzymes differ from HP1 and are not sensitive to compounds that impair liquid-liquid phase separation. Suv39h2 contains an N-terminal basic domain that is also present in around 23% of annotated Suv39h orthologs. The Suv39h2 basic domain provides resistance to chromatin-destabilizing agents, such as mitoxantrone and curaxin, and protects H3K9me3 heterochromatin from unfolding or chemically induced histone eviction. This protective function of the basic domain can be transferred to Suv39h1 as an N-terminal fusion. Together, these findings identify the Suv39h2 basic domain as a structural component of heterochromatin and suggest that basic domain extensions help to buffer heterochromatin destabilization. - Source: PubMed
Publication date: 2026/04/08
Świst-Rosowska Kalina MChing Reagan WKoschorz BirgitGalan CarmenEngist BettinaJenuwein Thomas - HT-2 toxin, a common grain contaminant, has been shown to impair mammalian reproductive function, but its specific effects on the epigenetic modifications of oocytes have not been systematically elucidated. This study aimed to investigate the impact of HT-2 toxin exposure on epigenetic modifications in mouse oocytes and the potential intervention of melatonin. The results revealed that HT-2 exposure downregulated the expression of histone methyltransferases (Suv39h2, Ehmt1, Ezh1, Ezh2) and the DNA demethylase Tet3, leading to reduced levels of repressive histone modifications (H3K9me3, H3K27me3) and abnormally elevated DNA methylation, which in turn compromised oocyte quality and significantly reduced the blastocyst formation rate after fertilization. The addition of melatonin effectively reversed the dysregulation of these epigenetics-related genes, restored histone modification and DNA methylation levels, and significantly improved embryonic developmental potential. This study reveals a novel mechanism by which melatonin mitigates reproductive toxicity through multi-target correction of HT-2-induced epigenetic errors, providing a potential strategy for preventing and addressing reproductive health issues caused by environmental toxins. - Source: PubMed
Publication date: 2026/04/21
Wu FeiQu HuiminJin Jun-XueZhang Ruimen