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  1. AU="Zhao, Chris Z"
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  1. Article: Cell cycle perturbation uncouples mitotic progression and invasive behavior in a post-mitotic cell.

    Martinez, Michael A Q / Zhao, Chris Z / Moore, Frances E Q / Yee, Callista / Zhang, Wan / Shen, Kang / Martin, Benjamin L / Matus, David Q

    bioRxiv : the preprint server for biology

    2024  

    Abstract: The acquisition of the post-mitotic state is crucial for the execution of many terminally differentiated cell behaviors during organismal development. However, the mechanisms that maintain the post-mitotic state in this context remain poorly understood. ... ...

    Abstract The acquisition of the post-mitotic state is crucial for the execution of many terminally differentiated cell behaviors during organismal development. However, the mechanisms that maintain the post-mitotic state in this context remain poorly understood. To gain insight into these mechanisms, we used the genetically and visually accessible model of
    Language English
    Publishing date 2024-02-07
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.03.16.533034
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Cell cycle perturbation uncouples mitotic progression and invasive behavior in a post-mitotic cell.

    Martinez, Michael A Q / Zhao, Chris Z / Moore, Frances E Q / Yee, Callista / Zhang, Wan / Shen, Kang / Martin, Benjamin L / Matus, David Q

    Differentiation; research in biological diversity

    2024  Volume 137, Page(s) 100765

    Abstract: The acquisition of the post-mitotic state is crucial for the execution of many terminally differentiated cell behaviors during organismal development. However, the mechanisms that maintain the post-mitotic state in this context remain poorly understood. ... ...

    Abstract The acquisition of the post-mitotic state is crucial for the execution of many terminally differentiated cell behaviors during organismal development. However, the mechanisms that maintain the post-mitotic state in this context remain poorly understood. To gain insight into these mechanisms, we used the genetically and visually accessible model of C. elegans anchor cell (AC) invasion into the vulval epithelium. The AC is a terminally differentiated uterine cell that normally exits the cell cycle and enters a post-mitotic state before initiating contact between the uterus and vulva through a cell invasion event. Here, we set out to identify the set of negative cell cycle regulators that maintain the AC in this post-mitotic, invasive state. Our findings revealed a critical role for CKI-1 (p21
    Language English
    Publishing date 2024-03-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 184540-8
    ISSN 1432-0436 ; 0301-4681
    ISSN (online) 1432-0436
    ISSN 0301-4681
    DOI 10.1016/j.diff.2024.100765
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1170: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
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  3. Article ; Online: An expandable FLP-ON::TIR1 system for precise spatiotemporal protein degradation in Caenorhabditis elegans.

    Xiao, Yutong / Yee, Callista / Zhao, Chris Z / Martinez, Michael A Q / Zhang, Wan / Shen, Kang / Matus, David Q / Hammell, Christopher

    Genetics

    2023  Volume 223, Issue 4

    Abstract: The auxin-inducible degradation system has been widely adopted in the Caenorhabditis elegans research community for its ability to empirically control the spatiotemporal expression of target proteins. This system can efficiently degrade auxin-inducible ... ...

    Abstract The auxin-inducible degradation system has been widely adopted in the Caenorhabditis elegans research community for its ability to empirically control the spatiotemporal expression of target proteins. This system can efficiently degrade auxin-inducible degron (AID)-tagged proteins via the expression of a ligand-activatable AtTIR1 protein derived from A. thaliana that adapts target proteins to the endogenous C. elegans proteasome. While broad expression of AtTIR1 using strong, ubiquitous promoters can lead to rapid degradation of AID-tagged proteins, cell type-specific expression of AtTIR1 using spatially restricted promoters often results in less efficient target protein degradation. To circumvent this limitation, we have developed an FLP/FRT3-based system that functions to reanimate a dormant, high-powered promoter that can drive sufficient AtTIR1 expression in a cell type-specific manner. We benchmark the utility of this system by generating a number of tissue-specific FLP-ON::TIR1 drivers to reveal genetically separable cell type-specific phenotypes for several target proteins. We also demonstrate that the FLP-ON::TIR1 system is compatible with enhanced degron epitopes. Finally, we provide an expandable toolkit utilizing the basic FLP-ON::TIR1 system that can be adapted to drive optimized AtTIR1 expression in any tissue or cell type of interest.
    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Indoleacetic Acids/metabolism ; Proteasome Endopeptidase Complex/genetics ; Proteasome Endopeptidase Complex/metabolism ; Proteins/metabolism ; Proteolysis ; Arabidopsis Proteins
    Chemical Substances Indoleacetic Acids ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Proteins ; Arabidopsis Proteins
    Language English
    Publishing date 2023-01-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2167-2
    ISSN 1943-2631 ; 0016-6731
    ISSN (online) 1943-2631
    ISSN 0016-6731
    DOI 10.1093/genetics/iyad013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 767: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Reevaluating the relationship between EGL-43 (EVI1) and LIN-12 (Notch) during C. elegans anchor cell invasion.

    Martinez, Michael A Q / Mullarkey, Angelina A / Yee, Callista / Zhao, Chris Z / Zhang, Wan / Shen, Kang / Matus, David Q

    Biology open

    2022  Volume 11, Issue 12

    Abstract: Development of the Caenorhabditis elegans reproductive tract is orchestrated by the anchor cell (AC). This occurs in part through a cell invasion event that connects the uterine and vulval tissues. Several key transcription factors regulate AC invasion, ... ...

    Abstract Development of the Caenorhabditis elegans reproductive tract is orchestrated by the anchor cell (AC). This occurs in part through a cell invasion event that connects the uterine and vulval tissues. Several key transcription factors regulate AC invasion, such as EGL-43, HLH-2, and NHR-67. Specifically, these transcription factors function together to maintain the post-mitotic state of the AC, a requirement for AC invasion. Recently, a mechanistic connection has been made between loss of EGL-43 and AC cell-cycle entry. The current model states that EGL-43 represses LIN-12 (Notch) expression to prevent AC proliferation, suggesting that Notch signaling has mitogenic effects in the invasive AC. To reexamine the relationship between EGL-43 and LIN-12, we first designed and implemented a heterologous co-expression system called AIDHB that combines the auxin-inducible degron (AID) system of plants with a live cell-cycle sensor based on human DNA helicase B (DHB). After validating AIDHB using AID-tagged GFP, we sought to test it by using AID-tagged alleles of egl-43 and lin-12. Auxin-induced degradation of either EGL-43 or LIN-12 resulted in the expected AC phenotypes. Lastly, we seized the opportunity to pair AIDHB with RNAi to co-deplete LIN-12 and EGL-43, respectively, which revealed that LIN-12 is not required for AC proliferation following loss of EGL-43.
    MeSH term(s) Animals ; Female ; Humans ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/metabolism ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Indoleacetic Acids/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Vulva/metabolism
    Chemical Substances Basic Helix-Loop-Helix Transcription Factors ; Caenorhabditis elegans Proteins ; HLH-2 protein, C elegans ; Indoleacetic Acids ; Lin-12 protein, C elegans ; Nhr-67 protein, C elegans ; Receptors, Cytoplasmic and Nuclear ; Receptors, Notch ; Transcription Factors ; Egl-43 protein, C elegans
    Language English
    Publishing date 2022-12-06
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2632264-X
    ISSN 2046-6390 ; 2046-6390
    ISSN (online) 2046-6390
    ISSN 2046-6390
    DOI 10.1242/bio.059668
    Database MEDical Literature Analysis and Retrieval System OnLINE

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