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  1. Article ; Online: Kinesin-1 transports morphologically distinct intracellular virions during vaccinia infection.

    Xu, Amadeus / Basant, Angika / Schleich, Sibylle / Newsome, Timothy P / Way, Michael

    Journal of cell science

    2022  Volume 136, Issue 5

    Abstract: Intracellular mature viruses (IMVs) are the first and most abundant infectious form of vaccinia virus to assemble during its replication cycle. IMVs can undergo microtubule-based motility, but their directionality and the motor involved in their ... ...

    Abstract Intracellular mature viruses (IMVs) are the first and most abundant infectious form of vaccinia virus to assemble during its replication cycle. IMVs can undergo microtubule-based motility, but their directionality and the motor involved in their transport remain unknown. Here, we demonstrate that IMVs, like intracellular enveloped viruses (IEVs), the second form of vaccinia that are wrapped in Golgi-derived membranes, recruit kinesin-1 and undergo anterograde transport. In vitro reconstitution of virion transport in infected cell extracts revealed that IMVs and IEVs move toward microtubule plus ends with respective velocities of 0.66 and 0.56 µm/s. Quantitative imaging established that IMVs and IEVs recruit an average of 139 and 320 kinesin-1 motor complexes, respectively. In the absence of kinesin-1, there was a near-complete loss of in vitro motility and reduction in the intracellular spread of both types of virions. Our observations demonstrate that kinesin-1 transports two morphologically distinct forms of vaccinia. Reconstitution of vaccinia-based microtubule motility in vitro provides a new model to elucidate how motor number and regulation impacts transport of a bona fide kinesin-1 cargo.
    MeSH term(s) Cell Extracts ; Humans ; Kinesins ; Microtubules/metabolism ; Vaccinia/metabolism ; Vaccinia virus ; Virion/physiology
    Chemical Substances Cell Extracts ; Kinesins (EC 3.6.4.4)
    Language English
    Publishing date 2022-09-30
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.260175
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 14: Show issues

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  2. Article ; Online: Regulator of calcineurin-2 is a centriolar protein with a role in cilia length control.

    Stevenson, Nicola L / Bergen, Dylan J M / Xu, Amadeus / Wyatt, Emily / Henry, Freya / McCaughey, Janine / Vuolo, Laura / Hammond, Chrissy L / Stephens, David J

    Journal of cell science

    2018  Volume 131, Issue 9

    Abstract: Almost every cell in the human body extends a primary cilium. Defective cilia function leads to a set of disorders known as ciliopathies, which are characterised by debilitating developmental defects that affect many tissues. Here, we report a new role ... ...

    Abstract Almost every cell in the human body extends a primary cilium. Defective cilia function leads to a set of disorders known as ciliopathies, which are characterised by debilitating developmental defects that affect many tissues. Here, we report a new role for regulator of calcineurin 2 (RCAN2) in primary cilia function. It localises to centrioles and the basal body and is required to maintain normal cilia length. RCAN2 was identified as the most strongly upregulated gene from a comparative RNAseq analysis of cells in which expression of the Golgi matrix protein giantin had been abolished by gene editing. In contrast to previous work where we showed that depletion of giantin by RNAi results in defects in ciliogenesis and in cilia length control, giantin knockout cells generate normal cilia after serum withdrawal. Furthermore, giantin knockout zebrafish show increased expression of RCAN2. Importantly, suppression of RCAN2 expression in giantin knockout cells results in the same defects in the control of cilia length that are seen upon RNAi of giantin itself. Together, these data define RCAN2 as a regulator of cilia function that can compensate for the loss of giantin function.
    MeSH term(s) Animals ; Cell Cycle Proteins/metabolism ; Centrioles/genetics ; Centrioles/metabolism ; Cilia/genetics ; Cilia/metabolism ; Gene Knockout Techniques ; Golgi Matrix Proteins/genetics ; Golgi Matrix Proteins/metabolism ; Humans ; Muscle Proteins/genetics ; Muscle Proteins/metabolism ; Retinal Pigment Epithelium/cytology ; Retinal Pigment Epithelium/metabolism ; Zebrafish
    Chemical Substances Cell Cycle Proteins ; Golgi Matrix Proteins ; Muscle Proteins ; RCAN2 protein, human ; macrogolgin
    Language English
    Publishing date 2018-05-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2993-2
    ISSN 1477-9137 ; 0021-9533
    ISSN (online) 1477-9137
    ISSN 0021-9533
    DOI 10.1242/jcs.212258
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 1200: 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)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 14: Show issues

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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