MICAL-L1-related and unrelated mechanisms underlying elongated tubular endosomal network (ETEN) in human dendritic cells

Journal article

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: Compeer, E; Boes, M

• Publication status: Published
• Peer review status: Peer reviewed
• Publisher: Taylor and Francis
• Journal: Communicative and Integrative Biology
• Volume: 7
• Issue: 6
• Pages: e994969
• Publication date: 2014-12-23
• Acceptance date: 2014-07-29
• DOI: 10.4161/19420889.2014.994969
• ISSN: 1942-0889
• Language: English
• Keywords: endosomal recycling; MICALL1; membrane remodeling; SBTMR; elongated tubular endosomal network (ETEN)