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Article ; Online: Author Correction: Distinct dynamics and functions of H2AK119ub1 and H3K27me3 in mouse preimplantation embryos.

Chen, Zhiyuan / Djekidel, Mohamed Nadhir / Zhang, Yi

2021 Volume 53, Issue 6, Page(s) 936

Language	English
Publishing date	2021-04-22
Publishing country	United States
Document type	Published Erratum
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-021-00871-6
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Zs.A 3613: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 46: Show issues

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Article ; Online: Spatial transcriptomics reveals the distinct organization of mouse prefrontal cortex and neuronal subtypes regulating chronic pain.

Bhattacherjee, Aritra / Zhang, Chao / Watson, Brianna R / Djekidel, Mohamed Nadhir / Moffitt, Jeffrey R / Zhang, Yi

Nature neuroscience

2023 Volume 26, Issue 11, Page(s) 1880–1893

Abstract: The prefrontal cortex (PFC) is a complex brain region that regulates diverse functions ranging from cognition, emotion and executive action to even pain processing. To decode the cellular and circuit organization of such diverse functions, we employed ... ...

Abstract	The prefrontal cortex (PFC) is a complex brain region that regulates diverse functions ranging from cognition, emotion and executive action to even pain processing. To decode the cellular and circuit organization of such diverse functions, we employed spatially resolved single-cell transcriptome profiling of the adult mouse PFC. Results revealed that PFC has distinct cell-type composition and gene-expression patterns relative to neighboring cortical areas-with neuronal excitability-regulating genes differently expressed. These cellular and molecular features are further segregated within PFC subregions, alluding to the subregion-specificity of several PFC functions. PFC projects to major subcortical targets through combinations of neuronal subtypes, which emerge in a target-intrinsic fashion. Finally, based on these features, we identified distinct cell types and circuits in PFC underlying chronic pain, an escalating healthcare challenge with limited molecular understanding. Collectively, this comprehensive map will facilitate decoding of discrete molecular, cellular and circuit mechanisms underlying specific PFC functions in health and disease.
MeSH term(s)	Mice ; Animals ; Transcriptome ; Chronic Pain/genetics ; Cognition/physiology ; Prefrontal Cortex/physiology ; Gene Expression Profiling
Language	English
Publishing date	2023-10-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/s41593-023-01455-9
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Zs.A 4891: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 67: Show issues

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Article ; Online: Distinct dynamics and functions of H2AK119ub1 and H3K27me3 in mouse preimplantation embryos.

Chen, Zhiyuan / Djekidel, Mohamed Nadhir / Zhang, Yi

Nature genetics

2021 Volume 53, Issue 4, Page(s) 551–563

Abstract: Polycomb repressive complexes 1 and 2 (PRC1/2) maintain transcriptional silencing of developmental genes largely by catalyzing the formation of mono-ubiquitinated histone H2A at lysine 119 (H2AK119ub1) and trimethylated histone H3 at lysine 27 (H3K27me3), ...

Abstract	Polycomb repressive complexes 1 and 2 (PRC1/2) maintain transcriptional silencing of developmental genes largely by catalyzing the formation of mono-ubiquitinated histone H2A at lysine 119 (H2AK119ub1) and trimethylated histone H3 at lysine 27 (H3K27me3), respectively. How Polycomb domains are reprogrammed during mammalian preimplantation development remains largely unclear. Here we show that, although H2AK119ub1 and H3K27me3 are highly colocalized in gametes, they undergo differential reprogramming dynamics following fertilization. H3K27me3 maintains thousands of maternally biased domains until the blastocyst stage, whereas maternally biased H2AK119ub1 distribution in zygotes is largely equalized at the two-cell stage. Notably, while maternal PRC2 depletion has a limited effect on global H2AK119ub1 in early embryos, it disrupts allelic H2AK119ub1 at H3K27me3 imprinting loci including Xist. By contrast, acute H2AK119ub1 depletion in zygotes does not affect H3K27me3 imprinting maintenance, at least by the four-cell stage. Importantly, loss of H2AK119ub1, but not H3K27me3, causes premature activation of developmental genes during zygotic genome activation (ZGA) and subsequent embryonic arrest. Thus, our study reveals distinct dynamics and functions of H3K27me3 and H2AK119ub1 in mouse preimplantation embryos.
MeSH term(s)	Animals ; Blastocyst/cytology ; Blastocyst/metabolism ; Epigenesis, Genetic ; Female ; Fertilization/genetics ; Gene Expression Regulation, Developmental ; Histones/genetics ; Histones/metabolism ; Lysine/metabolism ; Male ; Maternal Inheritance ; Mice ; Oocytes/cytology ; Oocytes/growth & development ; Oocytes/metabolism ; Paternal Inheritance ; Polycomb Repressive Complex 1/genetics ; Polycomb Repressive Complex 1/metabolism ; Polycomb Repressive Complex 2/genetics ; Polycomb Repressive Complex 2/metabolism ; Pregnancy ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Spermatozoa/cytology ; Spermatozoa/metabolism ; Ubiquitination ; Zygote/cytology ; Zygote/growth & development ; Zygote/metabolism
Chemical Substances	Histones ; Protein Isoforms ; RNA, Long Noncoding ; XIST non-coding RNA ; Polycomb Repressive Complex 2 (EC 2.1.1.43) ; Polycomb Repressive Complex 1 (EC 2.3.2.27) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2021-04-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-021-00821-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Zs.A 3613: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: A transcriptional roadmap for 2C-like-to-pluripotent state transition.

Fu, Xudong / Djekidel, Mohamed Nadhir / Zhang, Yi

Science advances

2020 Volume 6, Issue 22, Page(s) eaay5181

Abstract: In mouse embryonic stem cell (ESC), a small cell population displays totipotent features by expressing a set of genes that are transiently active in 2-cell-stage embryos. These 2-cell-like (2C-like) cells spontaneously transit back into the pluripotent ... ...

Abstract	In mouse embryonic stem cell (ESC), a small cell population displays totipotent features by expressing a set of genes that are transiently active in 2-cell-stage embryos. These 2-cell-like (2C-like) cells spontaneously transit back into the pluripotent state. We previously dissected the transcriptional dynamics of the transition from pluripotency to the totipotent 2C-like state and identified factors that modulate the process. However, how 2C-like cells transit back into the pluripotent state remains largely unknown. In this study, we analyzed the transcriptional dynamics from the 2C-like state to pluripotent ESCs and identified an intermediate state. The intermediate state characterized by two-wave step up-regulation of pluripotent genes is different from the one observed during the 2C-like entry transition. Nonsense-mediated Dux mRNA decay plays an important role in the 2C-like state exit. Thus, our study not only provides a transcriptional roadmap for 2C-like-to-pluripotent state transition but also reveals a key molecular event driving the transition.
Keywords	covid19
Language	English
Publishing date	2020-05-29
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.aay5181
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Auxin-inducible degron 2 system deciphers functions of CTCF domains in transcriptional regulation.

Hyle, Judith / Djekidel, Mohamed Nadhir / Williams, Justin / Wright, Shaela / Shao, Ying / Xu, Beisi / Li, Chunliang

Genome biology

2023 Volume 24, Issue 1, Page(s) 14

Abstract: Background: CTCF is a well-established chromatin architectural protein that also plays various roles in transcriptional regulation. While CTCF biology has been extensively studied, how the domains of CTCF function to regulate transcription remains ... ...

Abstract	Background: CTCF is a well-established chromatin architectural protein that also plays various roles in transcriptional regulation. While CTCF biology has been extensively studied, how the domains of CTCF function to regulate transcription remains unknown. Additionally, the original auxin-inducible degron 1 (AID1) system has limitations in investigating the function of CTCF. Results: We employ an improved auxin-inducible degron technology, AID2, to facilitate the study of acute depletion of CTCF while overcoming the limitations of the previous AID system. As previously observed through the AID1 system and steady-state RNA analysis, the new AID2 system combined with SLAM-seq confirms that CTCF depletion leads to modest nascent and steady-state transcript changes. A CTCF domain sgRNA library screening identifies the zinc finger (ZF) domain as the region within CTCF with the most functional relevance, including ZFs 1 and 10. Removal of ZFs 1 and 10 reveals genomic regions that independently require these ZFs for DNA binding and transcriptional regulation. Notably, loci regulated by either ZF1 or ZF10 exhibit unique CTCF binding motifs specific to each ZF. Conclusions: By extensively comparing the AID1 and AID2 systems for CTCF degradation in SEM cells, we confirm that AID2 degradation is superior for achieving miniAID-tagged protein degradation without the limitations of the AID1 system. The model we create that combines AID2 depletion of CTCF with exogenous overexpression of CTCF mutants allows us to demonstrate how peripheral ZFs intricately orchestrate transcriptional regulation in a cellular context for the first time.
MeSH term(s)	CCCTC-Binding Factor/metabolism ; Indoleacetic Acids ; Gene Expression Regulation ; Zinc Fingers ; Genome
Chemical Substances	CCCTC-Binding Factor ; Indoleacetic Acids
Language	English
Publishing date	2023-01-26
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2040529-7
ISSN	1474-760X ; 1474-760X
ISSN (online)	1474-760X
ISSN	1474-760X
DOI	10.1186/s13059-022-02843-3
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Article ; Online: Auxin-inducible degron 2 system deciphers functions of CTCF domains in transcriptional regulation

Judith Hyle / Mohamed Nadhir Djekidel / Justin Williams / Shaela Wright / Ying Shao / Beisi Xu / Chunliang Li

Genome Biology, Vol 24, Iss 1, Pp 1-

2023 Volume 30

Abstract: Abstract Background CTCF is a well-established chromatin architectural protein that also plays various roles in transcriptional regulation. While CTCF biology has been extensively studied, how the domains of CTCF function to regulate transcription ... ...

Abstract	Abstract Background CTCF is a well-established chromatin architectural protein that also plays various roles in transcriptional regulation. While CTCF biology has been extensively studied, how the domains of CTCF function to regulate transcription remains unknown. Additionally, the original auxin-inducible degron 1 (AID1) system has limitations in investigating the function of CTCF. Results We employ an improved auxin-inducible degron technology, AID2, to facilitate the study of acute depletion of CTCF while overcoming the limitations of the previous AID system. As previously observed through the AID1 system and steady-state RNA analysis, the new AID2 system combined with SLAM-seq confirms that CTCF depletion leads to modest nascent and steady-state transcript changes. A CTCF domain sgRNA library screening identifies the zinc finger (ZF) domain as the region within CTCF with the most functional relevance, including ZFs 1 and 10. Removal of ZFs 1 and 10 reveals genomic regions that independently require these ZFs for DNA binding and transcriptional regulation. Notably, loci regulated by either ZF1 or ZF10 exhibit unique CTCF binding motifs specific to each ZF. Conclusions By extensively comparing the AID1 and AID2 systems for CTCF degradation in SEM cells, we confirm that AID2 degradation is superior for achieving miniAID-tagged protein degradation without the limitations of the AID1 system. The model we create that combines AID2 depletion of CTCF with exogenous overexpression of CTCF mutants allows us to demonstrate how peripheral ZFs intricately orchestrate transcriptional regulation in a cellular context for the first time.
Keywords	CTCF ; Transcription ; Auxin-inducible degron ; CRISPR ; Biology (General) ; QH301-705.5 ; Genetics ; QH426-470
Subject code	570
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: FIND: difFerential chromatin INteractions Detection using a spatial Poisson process.

Djekidel, Mohamed Nadhir / Chen, Yang / Zhang, Michael Q

Genome research

2018

Abstract: Polymer-based simulations and experimental studies indicate the existence of a spatial dependency between the adjacent DNA fibers involved in the formation of chromatin loops. However, the existing strategies for detecting differential chromatin ... ...

Abstract	Polymer-based simulations and experimental studies indicate the existence of a spatial dependency between the adjacent DNA fibers involved in the formation of chromatin loops. However, the existing strategies for detecting differential chromatin interactions assume that the interacting segments are spatially independent from the other segments nearby. To resolve this issue, we developed a new computational method, FIND, which considers the local spatial dependency between interacting loci. FIND uses a spatial Poisson process to detect differential chromatin interactions that show a significant difference in their interaction frequency and the interaction frequency of their neighbors. Simulation and biological data analysis show that FIND outperforms the widely used count-based methods and has a better signal-to-noise ratio.
Language	English
Publishing date	2018-02-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	1284872-4
ISSN	1549-5469 ; 1088-9051 ; 1054-9803
ISSN (online)	1549-5469
ISSN	1088-9051 ; 1054-9803
DOI	10.1101/gr.212241.116
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Zs.A 3729: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Interrogating bromodomain inhibitor resistance in KMT2A-rearranged leukemia through combinatorial CRISPR screens.

Wright, Shaela / Hu, Jianzhong / Wang, Hong / Hyle, Judith / Zhang, Yang / Du, Guoqing / Konopleva, Marina Y / Kornblau, Steven M / Djekidel, Mohamed Nadhir / Rosikiewicz, Wojciech / Xu, Beisi / Lu, Rui / Yang, Jun J / Li, Chunliang

Proceedings of the National Academy of Sciences of the United States of America

2023 Volume 120, Issue 16, Page(s) e2220134120

Abstract: Bromo- and extra-terminal domain inhibitors (BETi) have exhibited therapeutic activities in many cancers. However, the mechanisms controlling BETi response and resistance are not well understood. We conducted genome-wide loss-of-function CRISPR screens ... ...

Abstract	Bromo- and extra-terminal domain inhibitors (BETi) have exhibited therapeutic activities in many cancers. However, the mechanisms controlling BETi response and resistance are not well understood. We conducted genome-wide loss-of-function CRISPR screens using BETi-treated KMT2A-rearranged (KMT2A-r) cell lines. We revealed that
MeSH term(s)	Humans ; Clustered Regularly Interspaced Short Palindromic Repeats ; Glycogen Synthase Kinase 3/metabolism ; Cell Line, Tumor ; Leukemia/drug therapy ; Leukemia/genetics ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Repressor Proteins/metabolism
Chemical Substances	Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; SPOP protein, human ; Nuclear Proteins ; Repressor Proteins
Language	English
Publishing date	2023-04-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2220134120
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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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Article: A transcriptional roadmap for 2C-like-to-pluripotent state transition

Fu, Xudong / Djekidel, Mohamed Nadhir / Zhang, Yi

Sci. Adv

Abstract	In mouse embryonic stem cell (ESC), a small cell population displays totipotent features by expressing a set of genes that are transiently active in 2-cell-stage embryos. These 2-cell-like (2C-like) cells spontaneously transit back into the pluripotent state. We previously dissected the transcriptional dynamics of the transition from pluripotency to the totipotent 2C-like state and identified factors that modulate the process. However, how 2C-like cells transit back into the pluripotent state remains largely unknown. In this study, we analyzed the transcriptional dynamics from the 2C-like state to pluripotent ESCs and identified an intermediate state. The intermediate state characterized by two-wave step up-regulation of pluripotent genes is different from the one observed during the 2C-like entry transition. Nonsense-mediated Dux mRNA decay plays an important role in the 2C-like state exit. Thus, our study not only provides a transcriptional roadmap for 2C-like-to-pluripotent state transition but also reveals a key molecular event driving the transition.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #32937415
Database	COVID19

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