LYSOCIL CEDOC-NMS I FCM special seminar with Professor Rytis Prekeris
January 19, 2022 @Zoom
Special LYSOCIL CEDOC-NMS|FCM seminar with Rytis Prekeris, Professor of Cell and Developmental Biology, Director of Molecular Biology Graduate Program at School of Medicine, University of Colorado, Anschutz Medical Campus, USA will take place on January 19th, 2022, at 3 pm (Lisbon time) via Zoom. This seminar will be dedicated to “How to Make Apical Cilia: The Mechanisms Coordinating Ciliation and Epithelia Polarization".
Please request the link to: manage.lysocil@nms.unl.pt
Title: How to Make Apical Cilia: The Mechanisms Coordinating Ciliation and Epithelia Polarization
Abstract: One of the fundamental problems in cell biology is understanding how epithelial cells can function as a barrier, yet also receive and transport various molecules and signals important for tissue function and homeostasis. Epithelial cells exhibit remarkable apicobasal subcellular polarity that is essential for the proper tissue functioning and allows epithelial cells to form specialized structures such as apical primary cilia. Cilia also recently emerged as a key epithelial structure that mediates various aspects of cellular signaling and function. In this talk I will present our most recent work that starts dissecting the molecular machinery mediating ciliation in polarized epithelial cells.
LYSOCIL CEDOC-NMS I FCM special seminar with Professor Roberto Botelho
January 12, 2022 @Zoom
Special LYSOCIL CEDOC-NMS I FCM seminar with Dr. Roberto Botelho, Professor in the Department of Chemistry and Biology at Ryerson University in Toronto, Canada will take place on January 12, 2022, at 12 pm (Lisbon time) via Zoom. This seminar will be dedicated to "Putting the spotlight on phagosome resolution and phagocytic appetite".
Please request the link to: manage.lysocil@nms.unl.pt
Title: Putting the spotlight on phagosome resolution and phagocytic appetite
Abstract: In this talk, I will cover two related stories. First, I will review our recent work on the ultimate fate of phagosomes in macrophages. We discovered that phagosomes fragment after digesting the enclosed particles to reform lysosomes and maintain degradative capacity. This process is dependent on the cytoskeleton and clathrin machinery. We subsequently found that AP-2 complexes are also involved in recruiting clathrin to phagosomes and to help mediate phagosome resolution. A key question that remains unanswered is how is AP2-clathrin on phagosomes different, if they are, from endocytosis. Second, we began to investigate the processes that control phagocytic appetite. Our evidence shows that macrophages are able to sense when they have engulfed enough particles, however, little is known about how they do this. Our early work shows that this depends on phagosome resolution and recycling of endomembranes to offset cell shrinkage. We speculate that a key sensor for phagocytic appetite is tugour pressure, which may prevent remodelling of the plasma membrane during phagocytosis.
