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  1. Article ; Online: CUT & RUN to Profile Chromatin-Bound Proteins in Primary Mouse Neural Progenitor Cells.

    Matsui, Yurika / Peng, Jamy C

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2599, Page(s) 99–111

    Abstract: Cleavage under targets and release using nuclease (CUT & RUN) is an innovative method to profile histone modifications and chromatin-bound proteins genome-wide. CUT & RUN offers two distinct advantages of requiring much fewer cells and providing strong ... ...

    Abstract Cleavage under targets and release using nuclease (CUT & RUN) is an innovative method to profile histone modifications and chromatin-bound proteins genome-wide. CUT & RUN offers two distinct advantages of requiring much fewer cells and providing strong signal-to-noise ratios in deep-sequencing data. Here, we describe a workflow starting from dissociation and sorting of mouse embryonic brains, CUT & RUN, and DNA library preparation to deep sequencing. With our workflow, researchers can obtain high-quality sequencing data to profile histones and chromatin-associated proteins by using as few as 100,000 neural progenitor cells (NPCs).
    MeSH term(s) Mice ; Animals ; Chromatin/genetics ; Endonucleases/genetics ; Neural Stem Cells/metabolism ; Histones/metabolism ; Histone Code
    Chemical Substances Chromatin ; Endonucleases (EC 3.1.-) ; Histones
    Language English
    Publishing date 2022-11-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2847-8_8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Author Correction: Ybx1 fine-tunes PRC2 activities to control embryonic brain development.

    Evans, Myron K / Matsui, Yurika / Xu, Beisi / Willis, Catherine / Loome, Jennifer / Milburn, Luis / Fan, Yiping / Pagala, Vishwajeeth / Peng, Jamy C

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 412

    Language English
    Publishing date 2023-01-25
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-36069-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Author Correction

    Myron K. Evans / Yurika Matsui / Beisi Xu / Catherine Willis / Jennifer Loome / Luis Milburn / Yiping Fan / Vishwajeeth Pagala / Jamy C. Peng

    Nature Communications, Vol 14, Iss 1, Pp 1-

    Ybx1 fine-tunes PRC2 activities to control embryonic brain development

    2023  Volume 1

    Keywords Science ; Q
    Language English
    Publishing date 2023-01-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: SNIP1 and PRC2 coordinate cell fates of neural progenitors during brain development

    Yurika Matsui / Mohamed Nadhir Djekidel / Katherine Lindsay / Parimal Samir / Nina Connolly / Gang Wu / Xiaoyang Yang / Yiping Fan / Beisi Xu / Jamy C. Peng

    Nature Communications, Vol 14, Iss 1, Pp 1-

    2023  Volume 18

    Abstract: Abstract Stem cell survival versus death is a developmentally programmed process essential for morphogenesis, sizing, and quality control of genome integrity and cell fates. Cell death is pervasive during development, but its programming is little known. ...

    Abstract Abstract Stem cell survival versus death is a developmentally programmed process essential for morphogenesis, sizing, and quality control of genome integrity and cell fates. Cell death is pervasive during development, but its programming is little known. Here, we report that Smad nuclear interacting protein 1 (SNIP1) promotes neural progenitor cell survival and neurogenesis and is, therefore, integral to brain development. The SNIP1-depleted brain exhibits dysplasia with robust induction of caspase 9-dependent apoptosis. Mechanistically, SNIP1 regulates target genes that promote cell survival and neurogenesis, and its activities are influenced by TGFβ and NFκB signaling pathways. Further, SNIP1 facilitates the genomic occupancy of Polycomb complex PRC2 and instructs H3K27me3 turnover at target genes. Depletion of PRC2 is sufficient to reduce apoptosis and brain dysplasia and to partially restore genetic programs in the SNIP1-depleted brain in vivo. These findings suggest a loci-specific regulation of PRC2 and H3K27 marks to toggle cell survival and death in the developing brain.
    Keywords Science ; Q
    Subject code 571
    Language English
    Publishing date 2023-08-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: SNIP1 and PRC2 coordinate cell fates of neural progenitors during brain development.

    Matsui, Yurika / Djekidel, Mohamed Nadhir / Lindsay, Katherine / Samir, Parimal / Connolly, Nina / Wu, Gang / Yang, Xiaoyang / Fan, Yiping / Xu, Beisi / Peng, Jamy C

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 4754

    Abstract: Stem cell survival versus death is a developmentally programmed process essential for morphogenesis, sizing, and quality control of genome integrity and cell fates. Cell death is pervasive during development, but its programming is little known. Here, we ...

    Abstract Stem cell survival versus death is a developmentally programmed process essential for morphogenesis, sizing, and quality control of genome integrity and cell fates. Cell death is pervasive during development, but its programming is little known. Here, we report that Smad nuclear interacting protein 1 (SNIP1) promotes neural progenitor cell survival and neurogenesis and is, therefore, integral to brain development. The SNIP1-depleted brain exhibits dysplasia with robust induction of caspase 9-dependent apoptosis. Mechanistically, SNIP1 regulates target genes that promote cell survival and neurogenesis, and its activities are influenced by TGFβ and NFκB signaling pathways. Further, SNIP1 facilitates the genomic occupancy of Polycomb complex PRC2 and instructs H3K27me3 turnover at target genes. Depletion of PRC2 is sufficient to reduce apoptosis and brain dysplasia and to partially restore genetic programs in the SNIP1-depleted brain in vivo. These findings suggest a loci-specific regulation of PRC2 and H3K27 marks to toggle cell survival and death in the developing brain.
    MeSH term(s) Humans ; Intracellular Signaling Peptides and Proteins ; RNA-Binding Proteins ; Signal Transduction/physiology ; NF-kappa B ; Hyperplasia ; Brain
    Chemical Substances Intracellular Signaling Peptides and Proteins ; RNA-Binding Proteins ; NF-kappa B ; SNIP1 protein, human
    Language English
    Publishing date 2023-08-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-40487-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Phosphorylation of 53BP1 by ATM enforce neurodevelopmental programs in cortical organoids.

    Lim, Bitna / Djekidel, Mohamed Nadhir / Matsui, Yurika / Jung, Seunghyun / Yuan, Zuo-Fei / Wang, Xusheng / Yang, Xiaoyang / Pilehroud, Abbas Shirinifard / Pan, Haitao / Wang, Fang / Pruett-Miller, Shondra / Kavdia, Kanisha / Pagala, Vishwajeeth / Fan, Yiping / Peng, Junmin / Xu, Beisi / Peng, Jamy C

    bioRxiv : the preprint server for biology

    2023  

    Abstract: 53BP1 is a well-established DNA damage repair factor recently shown to regulate gene expression and critically influence tumor suppression and neural development. For gene regulation, how 53BP1 is regulated remains unclear. Here, we showed that 53BP1- ... ...

    Abstract 53BP1 is a well-established DNA damage repair factor recently shown to regulate gene expression and critically influence tumor suppression and neural development. For gene regulation, how 53BP1 is regulated remains unclear. Here, we showed that 53BP1-serine 25 phosphorylation by ATM is required for neural progenitor cell proliferation and neuronal differentiation in cortical organoids. 53BP1-serine 25 phosphorylation dynamics controls 53BP1 target genes for neuronal differentiation and function, cellular response to stress, and apoptosis. Beyond 53BP1, ATM is required for phosphorylation of factors in neuronal differentiation, cytoskeleton, p53 regulation, and ATM, BNDF, and WNT signaling pathways for cortical organoid differentiation. Overall, our data suggest that 53BP1 and ATM control key genetic programs required for human cortical development.
    Language English
    Publishing date 2023-05-04
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.05.04.539457
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Ybx1 fine-tunes PRC2 activities to control embryonic brain development

    Myron K. Evans / Yurika Matsui / Beisi Xu / Catherine Willis / Jennifer Loome / Luis Milburn / Yiping Fan / Vishwajeeth Pagala / Jamy C. Peng

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Volume 18

    Abstract: Polycomb repressive complex 2 (PRC2) methylates H3K27 and suppresses RNA polymerase II transcription by promoting a closed chromatin. Here the authors identify the transcription factor Ybx1 as an interactor that regulates the binding of PRC2 to chromatin ...

    Abstract Polycomb repressive complex 2 (PRC2) methylates H3K27 and suppresses RNA polymerase II transcription by promoting a closed chromatin. Here the authors identify the transcription factor Ybx1 as an interactor that regulates the binding of PRC2 to chromatin and H3K27 methylation to promote the genetic programs underlying neural lineages and neural progenitor self-renewal–differentiation choices.
    Keywords Science ; Q
    Language English
    Publishing date 2020-08-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article ; Online: Ybx1 fine-tunes PRC2 activities to control embryonic brain development

    Myron K. Evans / Yurika Matsui / Beisi Xu / Catherine Willis / Jennifer Loome / Luis Milburn / Yiping Fan / Vishwajeeth Pagala / Jamy C. Peng

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Volume 18

    Abstract: Polycomb repressive complex 2 (PRC2) methylates H3K27 and suppresses RNA polymerase II transcription by promoting a closed chromatin. Here the authors identify the transcription factor Ybx1 as an interactor that regulates the binding of PRC2 to chromatin ...

    Abstract Polycomb repressive complex 2 (PRC2) methylates H3K27 and suppresses RNA polymerase II transcription by promoting a closed chromatin. Here the authors identify the transcription factor Ybx1 as an interactor that regulates the binding of PRC2 to chromatin and H3K27 methylation to promote the genetic programs underlying neural lineages and neural progenitor self-renewal–differentiation choices.
    Keywords Science ; Q
    Language English
    Publishing date 2020-08-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  9. Article ; Online: Beyond transposons: the epigenetic and somatic functions of the Piwi-piRNA mechanism.

    Peng, Jamy C / Lin, Haifan

    Current opinion in cell biology

    2013  Volume 25, Issue 2, Page(s) 190–194

    Abstract: Piwi-interacting RNAs (piRNAs) were reported in 2006 as a novel class of small non-coding RNAs associated with Piwi proteins of the Argonaute/Piwi family. Recent studies have revealed not only the biogenesis of piRNAs and their roles in transposon ... ...

    Abstract Piwi-interacting RNAs (piRNAs) were reported in 2006 as a novel class of small non-coding RNAs associated with Piwi proteins of the Argonaute/Piwi family. Recent studies have revealed not only the biogenesis of piRNAs and their roles in transposon silencing, but also the function of the Piwi-piRNA pathway in epigenetic and post-transcriptional regulation of gene expression. In addition, the function of this pathway in somatic cells has also been more systematically characterized. The new findings reveal the Piwi-piRNA pathway as a more general mechanism of gene regulation.
    MeSH term(s) Animals ; Argonaute Proteins/metabolism ; DNA Transposable Elements/genetics ; Drosophila Proteins/metabolism ; Epigenesis, Genetic ; Gene Silencing ; Histones/chemistry ; Histones/metabolism ; RNA, Small Interfering/genetics ; RNA, Small Interfering/metabolism
    Chemical Substances Argonaute Proteins ; DNA Transposable Elements ; Drosophila Proteins ; Histones ; RNA, Small Interfering ; piwi protein, Drosophila
    Language English
    Publishing date 2013-03-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1026381-0
    ISSN 1879-0410 ; 0955-0674
    ISSN (online) 1879-0410
    ISSN 0955-0674
    DOI 10.1016/j.ceb.2013.01.010
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  10. Article ; Online: Ybx1 fine-tunes PRC2 activities to control embryonic brain development.

    Evans, Myron K / Matsui, Yurika / Xu, Beisi / Willis, Catherine / Loome, Jennifer / Milburn, Luis / Fan, Yiping / Pagala, Vishwajeeth / Peng, Jamy C

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 4060

    Abstract: Chromatin modifiers affect spatiotemporal gene expression programs that underlie organismal development. The Polycomb repressive complex 2 (PRC2) is a crucial chromatin modifier in executing neurodevelopmental programs. Here, we find that PRC2 interacts ... ...

    Abstract Chromatin modifiers affect spatiotemporal gene expression programs that underlie organismal development. The Polycomb repressive complex 2 (PRC2) is a crucial chromatin modifier in executing neurodevelopmental programs. Here, we find that PRC2 interacts with the nucleic acid-binding protein Ybx1. In the mouse embryo in vivo, Ybx1 is required for forebrain specification and restricting mid-hindbrain growth. In neural progenitor cells (NPCs), Ybx1 controls self-renewal and neuronal differentiation. Mechanistically, Ybx1 highly overlaps PRC2 binding genome-wide, controls PRC2 distribution, and inhibits H3K27me3 levels. These functions are consistent with Ybx1-mediated promotion of genes involved in forebrain specification, cell proliferation, or neuronal differentiation. In Ybx1-knockout NPCs, H3K27me3 reduction by PRC2 enzymatic inhibitor or genetic depletion partially rescues gene expression and NPC functions. Our findings suggest that Ybx1 fine-tunes PRC2 activities to regulate spatiotemporal gene expression in embryonic neural development and uncover a crucial epigenetic mechanism balancing forebrain-hindbrain lineages and self-renewal-differentiation choices in NPCs.
    MeSH term(s) Animals ; Blotting, Western ; Brain/embryology ; Brain/metabolism ; Cell Differentiation/genetics ; Cell Differentiation/physiology ; Cell Proliferation/genetics ; Cell Proliferation/physiology ; Cells, Cultured ; Chromatin Immunoprecipitation ; Drosophila ; Epigenesis, Genetic/genetics ; Flow Cytometry ; Fluorescent Antibody Technique ; Histone-Lysine N-Methyltransferase/genetics ; Histone-Lysine N-Methyltransferase/metabolism ; Immunoprecipitation ; Mice ; Mice, Knockout ; Protein Processing, Post-Translational/genetics ; Protein Processing, Post-Translational/physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Transcription Factors ; YB-1 protein, mouse ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
    Language English
    Publishing date 2020-08-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-17878-y
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