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RNA-seq analysis of Luciferase control-infected and DOT1L shRNA-infected primary cortical neurons.

ABSTRACT: We aimed to understand the transcriptional impact of partial loss of DOT1L in primary neurons from mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE272883 | GEO | 2025/11/13

REPOSITORIES: GEO

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RNA-seq analysis of Luciferase control-infected and DOT1L shRNA-infected primary cortical neurons.

Project description:RNA-seq analysis of Luciferase control-infected and DOT1L shRNA-infected primary cortical neurons.

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ChIP-seq analysis of control and DOT1L HET cortical nuclei.

Project description:We aimed to understand the changes in H3K79me2 deposition upon monoallelic DOT1L loss in cortical nuclei from 10 week old mice.

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single-nucleus transcriptomic analysis of cortical tissue from control and Dot1l HET 10 week old mice.

Project description:We aimed to understand the transcriptional impact of monoallelic loss of DOT1L in cortical nuclei from 10 week old mice.

2025-11-13 | GSE279120 | GEO

DOT1L deletion impairs the development of cortical Parvalbumin-expressing interneurons

Project description:Our group has reported that the histone methyltransferase DOT1L is necessary for proper cortical plate development and layer distribution of glutamatergic neurons, however, its specific role on cortical interneuron development has not yet been explored. Here, we demonstrate that DOT1L affects interneuron development in a cell-autonomous manner. Deletion of Dot1l in MGE-derived interneuron precursor cells results in an overall reduction and altered distribution of GABAergic interneurons in the cortical plate at postnatal day (P) 0. Furthermore, we observed an altered proportion of GABAergic interneurons in the cortex and striatum at P21 with a significant decrease in Parvalbumin (PVALB)-expressing interneurons. Altogether, our results indicate that reduced numbers of cortical interneurons upon DOT1L deletion results from altered postmitotic differentiation/maturation.

2023-08-01 | GSE221994 | GEO

Profiling of expression data in melanoma cells following DOT1L shRNA knockdown

Project description:DOT1L-dependent H3K79 methylation is associated with telomere silencing, meiotic checkpoint control, DNA repair, modulation of constitutive heterochromatin, and transcriptional activation.

2018-02-14 | GSE103080 | GEO

Differential gene expression of neuroblastoma cells stably expressing doxycycline-inducible DOT1L small hairpin RNA

Project description:We were interested in studying the role of DOT1L-mediated H3K79 methylation on N-Myc target gene transcription in MYCN-induced neuroblastoma. We aimed to determine whether knocking down DOT1L in MYCN-amplified neuroblastoma would affect N-Myc target gene expression.

2017-12-31 | GSE90585 | GEO

DOT1L regulates pericentromeric heterochromatin

Project description:Many repetitive DNA elements are packaged in heterochromatin, but depend on occasional transcription to maintain long-term silencing. The factors that promote transcription of repeat elements in heterochromatin are largely unknown. Here, we show that DOT1L, a histone methyltransferase that modifies lysine 79 of histone H3 (H3K79), is required for transcription of major satellite repeats to maintain pericentromeric heterochromatin (PCH), and that this function is essential for preimplantation development. DOT1L is a transcriptional activator at single-copy genes but does not have a known role in repeat element transcription. We show that H3K79me3 is specifically enriched at repetitive elements, that loss of DOT1L compromises pericentromeric major satellite transcription, and that this function depends on interaction between DOT1L and the chromatin remodeler SMARCA5. DOT1L inhibition causes chromosome breaks and cell cycle defects, and leads to embryonic lethality. Together, our findings uncover a vital new role for DOT1L in transcriptional activation of heterochromatic repeats.

2023-05-26 | PXD028824 | Pride

DOT1L inhibition exerts anti-tumor effects through activating interferon signaling in breast cancer cells

Project description:DOT1L, a histone H3 lysine 79 (H3K79) methyltransferase, is a potential therapeutic target in various malignancies. In the current study, we aimed to clarify the antitumor effect of DOT1L inhibition in breast cancer. Treatment with DOT1L inhibitors (SGC0942, EPZ-5676) suppressed proliferation and induced cell cycle arrest and apoptosis in estrogen receptor (ER)-positive/HER2-negative cancer cells (MCF7) as well as in ER-negative/HER2-positive cancer cells (SKBR3). Transcriptome and epigenome analysis revealed that DOT1L inhibition activated transcription of a number of interferon (IFN)-related genes (IRGs) in both cell lines. Our data suggest that the anti-breast cancer cell effect of DOT1L inhibition is mediated multiple mechanisms including activation of innate immune signaling.

2025-11-28 | GSE286942 | GEO

The Histone Methyltransferases MLL1 and DOT1L Cooperate with Meningioma-1 to Induce AML [Mouse Dot1l ko RNA-seq]

Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation of Dot1l or Mll1 in MN1 driven AML Methods: We sequenced mRNA from murine LSK-cells transformed using forced expression of MN1 (MSCV-MN1-IRES-GFP), and transduced with Cre-vector to inactivate either Dot1l or Mll1. Cells were sorted for Cre-expression (pTomato fluorescent marker) or expression of an inert control vector. Results: Inactivation of either Dot1l or Mll1 in this model leads to a substantial delay or complete abrogation of leukemia development. Loss of Dot1l or Mll1 are associated with gene expression changes that have substantial overlap. In addition, genes that are downregulated follwing inactivation of Dot1l or Mll1 have substantial overlap with the gene set upregulated in MN1 transduced CMPs. Conclusions: MN1 mediated leukemogenesis is associated with a gene expression program that dependes on Mll1 and Dot1l Examination of mRNA levels between Dot1l f/f and Dot1l ko, and Mll1 f/f and Mll1 ko.

2016-01-12 | E-GEOD-76748 | biostudies-arrayexpress

Profiling of expression data in melanoma cells with mutant DOT1L, DOT1L inhibitor or shRNA knockdown

Project description:Profiling of expression data in melanoma cells with mutant DOT1L, DOT1L inhibitor or shRNA knockdown

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