wipi-1 positive autophagosome-like vesicles entrap pathogenic staphylococcus aureus for lysosomal degradation

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ID: 209426
2012
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Ranked #36 of 61 articles by views in Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases

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Abstract
Invading pathogens provoke the autophagic machinery and, in a process termed xenophagy, the host cell survives because autophagy is employed as a safeguard for pathogens that escaped phagosomes. However, some pathogens can manipulate the autophagic pathway and replicate within the niche of generated autophagosome-like vesicles. By automated fluorescence-based high content analyses, we demonstrate that Staphylococcus aureus strains (USA300, HG001, SA113) stimulate autophagy and become entrapped in intracellular PtdIns(3)P-enriched vesicles that are decorated with human WIPI-1, an essential PtdIns(3)P effector of canonical autophagy and membrane protein of both phagophores and autophagosomes. Further, agr-positive S. aureus (USA300, HG001) strains were more efficiently entrapped in WIPI-1 positive autophagosome-like vesicles when compared to agr-negative cells (SA113). By confocal and electron microscopy we provide evidence that single- and multiple-Staphylococci entrapped undergo cell division. Moreover, the number of WIPI-1 positive autophagosome-like vesicles entrapping Staphylococci significantly increased upon (i) lysosomal inhibition by bafilomycin A1 and (ii) blocking PIKfyve-mediated PtdIns(3,5)P2 generation by YM201636. In summary, our results provide evidence that the PtdIns(3)P effector function of WIPI-1 is utilized during xenophagy of Staphylococcus aureus. We suggest that invading S. aureus cells become entrapped in autophagosome-like WIPI-1 positive vesicles targeted for lysosomal degradation in nonprofessional host cells.
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mauthe2012internationalwipi-1 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Mario Mauthe;Wenqi Yu;Oleg Krut;Martin Krönke;Friedrich Götz;Horst Robenek;Tassula Proikas-Cezanne
Journal Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases
Year 2012
DOI
10.1155/2012/179207
URL
http://dx.doi.org/10.1155/2012/179207
Keywords
cytology

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