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Edited By: Michael S. Marks, Trina A. Schroer, Robert G. Parton and Sharon A. Tooze

Online ISSN: 1600-0854

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  1. Global and local mechanisms sustain axonal proteostasis of transmembrane proteins

    Víctor Hugo Cornejo, Alejandro Luarte and Andrés Couve

    Version of Record online: 27 MAR 2017 | DOI: 10.1111/tra.12472

    Thumbnail image of graphical abstract

    Axonal proteostasis of membrane proteins is a complex phenomenon that involves post-Golgi vesicular transport (solid turquoise arrow and green membrane proteins), local translation/processing/trafficking (solid turquoise arrow and red membrane proteins), supply from supporting cells (dashed turquoise arrow and turquoise membrane proteins) and timely degradation (solid orange arrow). Although some of these mechanisms need further evidence or are currently somewhat speculative, the axon may be considered a system in which global and local phenomena interact to sustain function.

  2. C9orf72: At the intersection of lysosome cell biology and neurodegenerative disease

    Joseph Amick and Shawn M. Ferguson

    Version of Record online: 23 MAR 2017 | DOI: 10.1111/tra.12477

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    3 distinct mechanisms that have been proposed to explain how hexanucleotide repeat expansion within the C9orf72 gene causes neurodegeneration. (1) RNAs transcribed from the hexanucleotide repeat expansion form nuclear foci, which may trap key proteins involved in RNA processing. (2) Dipeptide repeat proteins produced by repeat associated non-AUG (RAN) translation form aggregates that may impair the function of membraneless organelles such as nucleoli and stress granules. Dipeptide repeat proteins may also disrupt transport through nuclear pores. (3) The repeat expansion also suppresses expression of the endogenous C9orf72 protein. Based on recent knockout studies, loss of C9orf72 is predicted to impair lysosome function This review focuses on recent progress toward elucidating lysosome-related functions for C9orf72.

  3. μ2-Dependent endocytosis of N-cadherin is regulated by β-catenin to facilitate neurite outgrowth

    Yi-ting Chen and Chin-Yin Tai

    Version of Record online: 23 MAR 2017 | DOI: 10.1111/tra.12473

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    Endocytosis of adhesion molecules is required for early neuronal development. Here we identified and characterized the mechanism controlling N-cadherin endocytosis through β-catenin-gated μ2/AP-2 binding to modulate neurite outgrowth.

  4. Routes and mechanisms of post-endosomal cholesterol trafficking: A story that never ends (pages 209–217)

    Jie Luo, Luyi Jiang, Hongyuan Yang and Bao-Liang Song

    Version of Record online: 21 MAR 2017 | DOI: 10.1111/tra.12471

    Thumbnail image of graphical abstract

    Post-endosomal cholesterol transport in a mammalian cell. Low-density lipoprotein (LDL) particles are taken up via LDL receptor (LDLR)-mediated endocytosis and delivered from early endosome (EE) to late endosome (LE)/lysosome (LY), during which LDL cholesteryl esters are hydrolyzed by acid lipase (AL) to release free cholesterol. Liberated cholesterol then exits LE/LY and moves to other organelles including the plasma membrane (PM), endoplasmic reticulum (ER), peroxisome (PERO), Golgi and mitochondria. These trafficking processes may involve nonvesicular transport at membrane contact sites formed by 2 closely apposed organelles. Upon reaching one membrane, cholesterol can be further delivered to another one, for example, the PM-to-ER retrograde cholesterol transport.

  5. HIV infection is influenced by dynamin at three independent points in the viral life cycle

    Anupriya Aggarwal, Tina L. Hitchen, Lars Ootes, Samantha McAllery, Andrew Wong, Khanh Nguyen, Adam McCluskey, Phillip J. Robinson and Stuart G. Turville

    Accepted manuscript online: 21 MAR 2017 01:45AM EST | DOI: 10.1111/tra.12481

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    Synopsis

    The concept that HIV endocytosis is the rate limiting step for HIV fusion in primary resting and activated CD4 T cell subsets has become controversial. Although dynamin plays a key role in endocytosis, modulation of its activity has led to both supportive and contradictory evidence for its role in HIV fusion. Through chemical dissection of dynamin action in the HIV life cycle of primary resting and activated CD4 T cells, we reveal that dynamin plays a role at three discrete stages: cell cycle related HIV transcription, the HIV fusion site and the HIV fusion reaction.

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