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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE138153 | GEO | 2020/10/01

REPOSITORIES: GEO

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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.

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Expression data from Sotos syndrome patients and controls

Project description:Genome-wide expression studies were performed on dermal fibroblasts from Sotos syndrome patients with a confirmed NSD1 abnormality and compared with age-sex matched controls. We used microarrays to detect differentially expressed genes in Sotos syndrome patients and performed a global test with the aim to map NSD1 within a signaling transduction pathway. Dermal fibroblasts were obtained from nine Sotos syndrome patients and nine controls. Since NSD1 is a co-factor of the retinoic acid receptor, cultures were performed both in the presence and absence of retinoic acid.

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Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in HepG2 cells: SETD2 knockdown and control cells

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Profiling of N6-methyladenosine in HepG2 cells: SETD2, METTL3, METTL14 or WTAP knockdown and control cells

Project description:SETD2 is the specific methyltransferase of H3K36me3, while METTL3, METTL14 and WTAP are the components of m6A methyltransferase complex. To understand the global effect of H3K36me3 on m6A modification, we compared the m6A profiling in SETD2 and METTL3, METTL14 or WTAP knockdown HepG2 cells, and found depletion of H3K36me3 by SETD2 silencing globally reduced m6A in human transcriptome. What’s more, most of the SETD2-dependent hypomethylation sites also responded to knockdown of METTL3, METTL14, or WTAP.

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SETD2 regulates the maternal epigenome, genomic imprinting and embryonic development [ChIP-seq]

Project description:The oocyte epigenome plays critical roles in mammalian gametogenesis and embryogenesis. Yet, how it is established remains elusive. Here, we report that histone-lysine N-methyltransferase SETD2, an H3K36me3 methyltransferase, is a crucial regulator of the mouse oocyte epigenome. Deficiency in Setd2 leads to extensive alterations of the oocyte epigenome, including the loss of H3K36me3, failure in establishing the correct DNA methylome, invasion of H3K4me3 and H3K27me3 into former H3K36me3 territories and aberrant acquisition of H3K4me3 at imprinting control regions instead of DNA methylation. Importantly, maternal depletion of SETD2 results in oocyte maturation defects and subsequent one-cell arrest after fertilization. The preimplantation arrest is mainly due to a maternal cytosolic defect, since it can be largely rescued by normal oocyte cytosol. However, chromatin defects, including aberrant imprinting, persist in these embryos, leading to embryonic lethality after implantation. Thus, these data identify SETD2 as a crucial player in establishing the maternal epigenome that in turn controls embryonic development.

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SETD2 regulates the maternal epigenome, genomic imprinting and embryonic development [Bisulfite-seq]

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Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in mouse embryonic stem cells: Setd2 knockdown and control cells

Project description:Setd2 is the specific methyltransferase of H3K36me3. To obtain Setd2-dependent landscape of H3K36me3 in mouse genome, we used mouse embryonic stem cells (mESCs) model with doxycycline (Dox)-induced Setd2 knockdown, and performed ChIP sequencing in mESCs with or without Dox treatment.

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Project description:Trimethylation of lysine 36 on histone H3 (H3K36me3), an epigenetic mark associated with actively transcribed genes, plays an important role in multiple cellular processes, including transcription elongation, DNA methylation, DNA repair, and RNA m6A methylation, etc. Aberrant expression and mutations of the main methyltransferase for H3K36me3, i.e., SET domain-containing 2 (SETD2), were shown to be associated with various cancers. Here, we performed targeted profiling of 154 epitranscriptomic RWE proteins using a scheduled liquid chromatography-parallel-reaction monitoring (LC-PRM) method coupled with the use of stable isotope-labeled (SIL) peptides as internal standards to investigate how H3K36me3 modulates the chromatin occupancies of epitranscriptomic reader, writer, and eraser (RWE) proteins. Our results showed consistent changes in chromatin occupancies of RWE proteins upon losses of H3K36me3 and H4K16ac, and a role of H3K36me3 in recruiting METTL3 to chromatin upon DNA double strand break induction. In addition, protein-protein interaction network and Kaplan-Meier survival analyses revealed the importance of METTL14 and TRMT11 in kidney cancer. Taken together, our work revealed cross-talks between H3K36me3 and epitranscriptomic RWE proteins and uncovered potential roles of these RWE proteins in H3K36me3-mediated biological processes.

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