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Traffic is a cell biology and biochemistry journal devoted to intracellular transport in health and disease, covering disciplines such as developmental biology, neuroscience, immunology, and infection in eukaryotes. We aim to publish manuscripts at the forefront of this field.
Papers provide insight into the mechanisms that underlie subcellular trafficking, membrane dynamics, and organelle function, and how these subcellular processes influence cellular physiology.
Call for Papers
“A Deadly Journey: Pathogen Trafficking through the Host Cell”
New team of Editors
A new team of Editors will take over at Traffic on January 2021. Please join us in welcoming Antonella De Matteis, Eeva-Liisa Eskelinen, Eric Chevet and Hesso Farhan.
Read here the introductory Editorial from the new team.
Please contact the editorial office ([email protected]) to extend the deadline for resubmission of a manuscript that is a result of delays in research progress that result from the current COVID-19 crisis.
Role of trafficking protein particle complex 2 in medaka development
-  14 November 2023
Mutations in TRAPPC2 (Sedlin) block collagen II export from the ER and cause the skeletal dysplasia called SEDT (spondyloepiphyseal dysplasia tarda). Here, we present the first vertebrate model for SEDT by knocking out the medaka orthologue OlSedl. The KO fish show a downregulation of collagen expression and exhibit a skeletal phenotype (platyspondyly/reduced length) that is highly reminiscent of that observed in SEDT patients, confirming that Sedlin plays a major role in skeletal development. Extraskeletal defects were also observed that involved the eye and the gut. Our data suggest that Sedlin is required for vertebrate embryo development by regulating collagen production and secretion in different tissues.
IST1 regulates select recycling pathways
-  5 November 2023
We report that ESCRT-III protein IST1 and its binding partner CHMP1B contribute to scission of endosomal carriers and that IST1 is required to efficiently deliver select cargo from early/sorting endosomes to recycling endosomes. IST1 also interacts with SNX15, and together they localize to a subdomain of early/sorting endosomes distinct from those known to be involved in recycling or degradation. SNX15 and CHMP1B alternately control recruitment of IST1 to different sites on the endosome, suggesting that IST1 plays multiple roles on early/sorting endosomes.
Sequence elements within the PEXEL motif and its downstream region modulate PTEX-dependent protein export in Plasmodium falciparum
-  5 November 2023
Peroxisome population control by phosphoinositide signaling at the endoplasmic reticulum-plasma membrane interface
-  5 November 2023
“How do cells regulate their organelle populations in response to environmental changes?” is a major question in cell biology. We show that regulation of peroxisome populations in yeast requires integrity of phosphatidylinositol-4-phosphate (PI4P) signaling at the cell cortex. When PI4P conversion to phoshatidylinositol (PI) is disrupted, PI4P increases in amount at the cell cortex, peroxisomes (red) detach from their cortical anchors (green) and the numbers of peroxisomes and their motility increase.
A new Caenorhabditis elegans model to study copper toxicity in Wilson disease
-  27 October 2023
C. elegans CUA-1 is an ortholog of human ATP7B, mutations in which cause Wilson disease (WD). The copper-transporting activity of CUA-1 counteracts copper toxicity by sequestering excess copper ions in lysosomes and promoting their efflux to the extracellular space. The substitution of a conserved histidine (H828Q) in CUA-1 recapitulates the most common ATP7B variant (H1069Q), causing WD. CUA-1 (H828Q) undergoes ER-associated degradation, thereby causing significant copper toxicity in mutant animals.