title: MICAL-L1-related and unrelated mechanisms underlying elongated tubular endosomal network (ETEN) in human dendritic cells.
abstract: The endosomal pathway constitutes a highly dynamic intracellular transport system, which is composed of vesicular and tubular compartments. Endosomal tubules enable geometry-based discrimination between membrane and luminal content. Extended tubular endosomes were suggested to deliver a steady stream of membrane proteins to one location more reliable and effective than vesicular endosomes. Recently, we demonstrated that human dendritic cells (DCs) form a large elongated tubular endosomal network, e.g. ETEN, upon distinct triggers. LPS-stimulation triggered late endosomal tubulation. Additional clustering of class I MHC and ICAM-1 by a cognate interaction between antigen-laden DC and antigen-specific CD8(+) T-cells induces formation of transferrin-positive tubules emanating from the endosomal recycling compartment (ERC). We here discuss cell-biological mechanisms that are involved in membrane bending and possibly underlie initiation, elongation, and stabilization of ETEN in human DCs. Using a knock-down approach we demonstrate that MICAL-L1 is necessary for ETEN remodeling originating from ERC in human DCs.
authors.affiliation: Department of Pediatrics; Laboratory of Translational Immunology; University Medical Center Utrecht; Wilhelmina Children's Hospital ; Utrecht, The Netherlands.
authors.forename: Ewoud B
authors.initials: EB
authors.lastname: Compeer
authors.affiliation: Department of Pediatrics; Laboratory of Translational Immunology; University Medical Center Utrecht; Wilhelmina Children's Hospital ; Utrecht, The Netherlands.
authors.forename: Marianne
authors.initials: M
authors.lastname: Boes
keywords: MICALL1; elongated tubular endosomal network (ETEN); endosomal recycling; membrane remodeling