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SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [ATAC-Seq]

ABSTRACT: Chromatin modifications are relevant for mammalian development, and their aberrant deposition is associated with human disease. While the mechanisms that deposit and remove these modifications have been largely elucidated, their role in regulating gene activity during cellular differentiation has yet to be completely understood. By differentiating a panel of mouse embryonic stem cells lacking major chromatin regulators towards neuronal cells, we identified their requirement at different stages of cellular differentiation. We show that the H3K36me3 methyltransferase SETD2 is important for the establishment of neuronal gene expression during late stages of differentiation but is dispensable once the cells have fully differentiated. While we don’t find evidence for a requirement of the histone methyltransferase activity in this process, we identify an indirect role of SETD2 in mediating interactions between the PAF1 complex and the elongating RNA Pol II, which could be required for optimal transcriptional processivity of neuronal genes.

ORGANISM(S): Mus musculus

PROVIDER: GSE278957 | GEO | 2026/05/20

REPOSITORIES: GEO

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SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [ChIP-Seq]

Project description:Chromatin modifications are relevant for mammalian development, and their aberrant deposition is associated with human disease. While the mechanisms that deposit and remove these modifications have been largely elucidated, their role in regulating gene activity during cellular differentiation has yet to be completely understood. By differentiating a panel of mouse embryonic stem cells lacking major chromatin regulators towards neuronal cells, we identified their requirement at different stages of cellular differentiation. We show that the H3K36me3 methyltransferase SETD2 is important for the establishment of neuronal gene expression during late stages of differentiation but is dispensable once the cells have fully differentiated. While we don’t find evidence for a requirement of the histone methyltransferase activity in this process, we identify an indirect role of SETD2 in mediating interactions between the PAF1 complex and the elongating RNA Pol II, which could be required for optimal transcriptional processivity of neuronal genes.

2026-05-20 | GSE278956 | GEO

SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [scRNA-Seq]

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SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [RNA-Seq]

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SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [ChIP-Seq]

Project description:SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [ChIP-Seq]

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SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [ATAC-Seq]

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SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [RNA-Seq]

Project description:SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [RNA-Seq]

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SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [scRNA-Seq]

Project description:SETD2 contributes to PAF1C interactions with the elongating RNA Pol II and is required for neuronal differentiation [scRNA-Seq]

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Comparison of gene expression pattern between Wild-type and Setd2 knockout mESCs [Affymetrix]

Project description:SETD2/HYPB has been known as a histone H3K36 specific methyltransferase. However, its roles in physiology such as development and cellular function remain unclear. In this study, using mESCs as cellular model, we show that Setd2 mainly regulates differentiation of murine embryonic stem cells (mESCs) towards primitive endoderm. This study aimed at exploring how did Setd2 regulate primitive endoderm. differentiation. We used microarrays to detail the global programme of gene expression controled by setd2, which is required for endoderm differentiation. Wild type and Setd2 knockout mESCs were selected for RNA extraction and hybridization on Affymetrix GeneChip® mouse genome 430 2.0 arrays. We sought to obtain some deregulated genes, which were required for primitive endoderm differentiation. For comparison, three biological repeats of each were performed.

2014-10-14 | E-GEOD-54931 | biostudies-arrayexpress

The methyltransferase activity of Setd2 is essential for mouse embryonic development: establishment of a mouse model harboring a patient-derived Setd2 mutation

Project description:The histone methyltransferase SETD2 is responsible for the transcription-coupled trimethylation of histone H3 lysine 36 (H3K36me3) on all protein-coding genes through its direct interaction with the elongating form of RNA polymerase II. In mice, Setd2 is required for embryonic development, as the Setd2-null mice are embryonic lethal due to impaired vascular remodeling. In human, SETD2 is frequently mutated in various types of cancer, thus representing one of the major chromatin-modification defects that drive tumorigenesis. Notably, recent studies suggest that, despite the central roles of their catalytic activities, many chromatin modifiers contain important non-catalytic (so-called “moonlighting”) functions, which are largely substantiated by their roles in protein-protein interactions. This notion is somewhat consistent with the observation that the cancer-associated SETD2 mutations are seemingly localized throughout the whole protein, thus raising a question whether the major function(s) of SETD2 is solely dependent on its methyltransferase activity. As an answer to this question, in this short report, we have established a site-specific Setd2 knock-in mouse model harboring a patient-derived, catalytic dead Setd2 and have provided clear evidence supporting that the requirement of Setd2 in mouse embryonic development is definitely dependent on its methyltransferase activity. However, it is also notable that, in comparison with the Setd2-null mice, the Setd2 catalytic dead mice showed slightly mild defects in embryonic development and gene expression changes, suggesting potential non-catalytic functions of Setd2, which could be studied in the future by using these different Setd2 mouse models.

2024-01-01 | GSE241154 | GEO

Abnormal neocortex arealization and Sotos-like syndrome-associated behavior in Setd2 mutant mice

Project description:Epigenetic regulation of gene expression through histone modifications like methylation of various lysine residues are essential for embryonic development. Here we removed SETD2, a methyltransferase for histone 3 lysine 36 trimethylation (H3K36me3), in the developing dorsal forebrain in mice and show it is required for proper area patterning (arealization) of the neocortex and the formation of thalamo-cortico-thalamic circuits by maintaining the expression of clustered protocadherin (Pcdh) genes in an H3K36me3 methyltransferase-dependent manner. Moreover, the Setd2 mutant mice exhibit defects in social interaction, motor endurance and spatial memory, reminiscent of patients with the Sotos-like syndrome bearing SETD2 mutations.

2020-10-01 | GSE138153 | GEO

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