IHEM   20887
INSTITUTO DE HISTOLOGIA Y EMBRIOLOGIA DE MENDOZA DR. MARIO H. BURGOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Galectins are present at the membrane of C. burnetii replicative vacuole
Autor/es:
MARIA EUGENIA MANSILLA PAREJA; MARIA ISABELCOLOMBO
Lugar:
Puerto Natales
Reunión:
Workshop; Current advances in membrane trafficking: Implications for polarity and diseases; 2014
Institución organizadora:
EMBO
Resumen:
Coxiella burnetii, the etiologic agent of Q fever, is a Gram-negative obligate intracellular bacterium. It has been previously described that both the endocytic and autophagic pathways contribute to Coxiella replicative vacuoles (CRV) maturation. Cumulative evidence indicate that autophagy protects the mammalian cytosol against bacterial infection. Efficient pathogen engulfment is mediated by cargo-selecting autophagy adaptors. This process relies on unidentified pattern- recognition or danger receptors to label invading pathogens as autophagy cargo, typically by polyubiquitin coating. Galectins are β-galactoside-binding lectins that accumulate in the cytosol before being secreted via a leader-peptide-independent pathway. It has been shown that Galectin 8 monitors endosomal and lysosomal integrity and detects bacterial invasion by binding host glycans exposed on damaged vacuoles. NDP52, nuclear dot protein 52 kDa, is an adaptor protein that binds both ubiquitin and LC3. In the present work, CHO cells transiently overexpressing several YFP- Galectins were infected with C. burnetii for different periods of time. By confocal microscopy, we observed the association of several YFP-Galectins and C. burnetii at different times after infection. Also we show that RFP-NDP52 interacts to CRV and this protein colocalizes with Gal-3 and Gal-8. Furthermore, both Galectins and NDP52 colocalize with LC3 in the CRVs. On the other hand, the presence of Galectins at the C. burnetii vacuole does not depend on autophagy modifications. Our results indicate that different adaptor molecules involved in key signaling pathways related to autophagy associate to the limiting membrane of CRV likely to control distinct host cell responses upon pathogen infection.