In:
mBio, American Society for Microbiology, Vol. 8, No. 4 ( 2017-09-06)
Abstract:
In epithelial cells, GAS can be efficiently killed within the lysosome-fused autophaosome compartment. However, we previously showed that, in spite of LC-3 recruitment, the autophagic machinery is not sufficient for GAS killing in endothelial cells. In this report, we provide the first evidence that Gal-3, highly expressed in endothelial cells, blocks the tagging of ubiquitin to GAS by inhibiting recruitment of Gal-8 and parkin, leading to an enhancement of GAS replication. We also provide the first demonstration that Gal-8 can interact with parkin, the critical E3 ligase, for resistance to intracellular bacteria by facilitating the decoration of bacteria with ubiquitin chains. Our findings reveal that differential levels of Gal-3 and Gal-8 expression and recruitment to GAS between epithelial cells and endothelial cells may contribute to the different outcomes of GAS elimination or survival and growth of GAS in these two types of cells.
Type of Medium:
Online Resource
ISSN:
2161-2129
,
2150-7511
DOI:
10.1128/mBio.00899-17
Language:
English
Publisher:
American Society for Microbiology
Publication Date:
2017
detail.hit.zdb_id:
2557172-2
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