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4 Research products, page 1 of 1

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  • A three-dimensional look into autophagy
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  • Open Access English
    Authors: 
    Mario Mauthe; Martijn A. Langereis; Jennifer Jung; Xingdong Zhou; Alex Jones; Wienand A. Omta; Sharon A. Tooze; Bjoern Stork; Søren R. Paludan; Tero Ahola; +6 more
    Publisher: The Rockefeller University Press
    Country: Netherlands
    Project: NWO | The role of autophagy in ... (2300175628), AKA | Mechanisms in the formati... (265997), NWO | A three-dimensional look ... (2300175771), NWO | Viral strategies to evade... (2300180032), WT , SNSF | ER-phagy mechanisms to ma... (154421), EC | XABA (282333)

    Autophagy is a catabolic process regulated by the orchestrated action of the autophagy-related (ATG) proteins. Recent work indicates that some of the ATG proteins also have autophagy-independent roles. Using an unbiased siRNA screen approach, we explored the extent of these unconventional functions of ATG proteins. We determined the effects of the depletion of each ATG proteome component on the replication of six different viruses. Our screen reveals that up to 36% of the ATG proteins significantly alter the replication of at least one virus in an unconventional fashion. Detailed analysis of two candidates revealed an undocumented role for ATG13 and FIP200 in picornavirus replication that is independent of their function in autophagy as part of the ULK complex. The high numbers of unveiled ATG gene-specific and pathogen-specific functions of the ATG proteins calls for caution in the interpretation of data, which rely solely on the depletion of a single ATG protein to specifically ablate autophagy. Autophagy-related (ATG) proteins regulate autophagy, but recent work indicates that some also have autophagy-independent roles. Here, Mauthe et al. perform an unbiased siRNA screen to examine the effects of ATG protein depletion on viral replication and demonstrate autophagy-independent functions for ATG13 and FIP200 in the picornaviral life cycle.

  • Other research product . Other ORP type . 2017
    Open Access English
    Authors: 
    Cong, Yingying; Verlhac, Pauline; Reggiori, Fulvio;
    Project: SNSF | ER-phagy mechanisms to ma... (154421), NWO | A three-dimensional look ... (2300175771), EC | PRONKJEWAIL (713660)

    Autophagy is a conserved intracellular catabolic pathway that allows cells to maintain homeostasis through the degradation of deleterious components via specialized double-membrane vesicles called autophagosomes. During the past decades, it has been revealed that numerous pathogens, including viruses, usurp autophagy in order to promote their propagation. Nidovirales are an order of enveloped viruses with large single-stranded positive RNA genomes. Four virus families (Arterividae, Coronaviridae, Mesoniviridae, and Roniviridae) are part of this order, which comprises several human and animal pathogens of medical and veterinary importance. In host cells, Nidovirales induce membrane rearrangements including autophagosome formation. The relevance and putative mechanism of autophagy usurpation, however, remain largely elusive. Here, we review the current knowledge about the possible interplay between Nidovirales and autophagy.

  • Open Access English
    Authors: 
    Alessia Landi; Muriel Mari; Tobias Wolf; Svenja Kleiser; Christine Gretzmeier; Isabel Wilhelm; Dimitra Kiritsi; Roland Thuenauer; Roger Geiger; Alexander Nyström; +3 more
    Publisher: Life Science Alliance LLC
    Country: Netherlands
    Project: EC | DRIVE (765912), NWO | A three-dimensional look ... (2300175771), EC | PRONKJEWAIL (713660), EC | LEC&LIP2INVADE (282105)

    Lectins are glycan-binding proteins with no catalytic activity and ubiquitously expressed in nature. Numerous bacteria use lectins to efficiently bind to epithelia, thus facilitating tissue colonisation. Wounded skin is one of the preferred niches for Pseudomonas aeruginosa, which has developed diverse strategies to impair tissue repair processes and promote infection. Here, we analyse the effect of the P. aeruginosa fucose-binding lectin LecB on human keratinocytes and demonstrate that it triggers events in the host, upon binding to fucosylated residues on cell membrane receptors, which extend beyond its role as an adhesion molecule. We found that LecB associates with insulin-like growth factor-1 receptor and dampens its signalling, leading to the arrest of cell cycle. In addition, we describe a novel LecB-triggered mechanism to down-regulate host cell receptors by showing that LecB leads to insulin-like growth factor-1 receptor internalisation and subsequent missorting towards intracellular endosomal compartments, without receptor activation. Overall, these data highlight that LecB is a multitask virulence factor that, through subversion of several host pathways, has a profound impact on keratinocyte proliferation and survival. This study provides a novel function of the bacterial lectin LecB, which dampens cell proliferation and survival by targeting the insulin-like growth factor-1 for degradation, without receptor activation.

  • Publication . Other literature type . Article . 2017
    Open Access English
    Authors: 
    Yingying Cong; Pauline Verlhac; Fulvio Reggiori;
    Publisher: MDPI
    Country: Netherlands
    Project: EC | PRONKJEWAIL (713660), SNSF | ER-phagy mechanisms to ma... (154421), NWO | A three-dimensional look ... (2300175771)

    Autophagy is a conserved intracellular catabolic pathway that allows cells to maintain homeostasis through the degradation of deleterious components via specialized double-membrane vesicles called autophagosomes. During the past decades, it has been revealed that numerous pathogens, including viruses, usurp autophagy in order to promote their propagation. Nidovirales are an order of enveloped viruses with large single-stranded positive RNA genomes. Four virus families (Arterividae, Coronaviridae, Mesoniviridae, and Roniviridae) are part of this order, which comprises several human and animal pathogens of medical and veterinary importance. In host cells, Nidovirales induce membrane rearrangements including autophagosome formation. The relevance and putative mechanism of autophagy usurpation, however, remain largely elusive. Here, we review the current knowledge about the possible interplay between Nidovirales and autophagy.