A Cilia Independent Role of Ift88/Polaris during Cell Migration

Ift88 is a central component of the intraflagellar transport (Ift) complex B, essential for the building of cilia and flagella from single cell organisms to mammals. Loss of Ift88 results in the absence of cilia and causes left-right asymmetry defects, disordered Hedgehog signaling, and polycystic k...

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Published in:PloS one 2015-10, Vol.10 (10), p.e0140378-e0140378
Main Authors: Boehlke, Christopher, Janusch, Heike, Hamann, Christoph, Powelske, Christian, Mergen, Miriam, Herbst, Henriette, Kotsis, Fruzsina, Nitschke, Roland, Kuehn, E Wolfgang
Format: Article
Language:English
Subjects:
Animals
Antibiotics
Carrier Proteins - metabolism
Cell adhesion & migration
Cell cycle
Cell division
Cell migration
Cell Movement
Cell Polarity
Cilia
Dogs
Experiments
Fibroblasts
Flagella
Flagella - metabolism
Hedgehog protein
Immunological synapses
Immunology
Kidney diseases
Kidneys
Kinesin
Kinesin - metabolism
Lymphocytes T
Madin Darby Canine Kidney Cells
Mitosis
Nephrology
Polycystic kidney
Proteins
Signal transduction
Synapses
T cell receptors
T cells
T-cell receptor
Wound healing
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cited_by cdi_FETCH-LOGICAL-c692t-363d38f216791213d87ad972f12ac4f9de25ffea29e41d05ab3bcd284906066e3
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container_end_page e0140378
container_issue 10
container_start_page e0140378
container_title PloS one
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creator Boehlke, Christopher
Janusch, Heike
Hamann, Christoph
Powelske, Christian
Mergen, Miriam
Herbst, Henriette
Kotsis, Fruzsina
Nitschke, Roland
Kuehn, E Wolfgang
description Ift88 is a central component of the intraflagellar transport (Ift) complex B, essential for the building of cilia and flagella from single cell organisms to mammals. Loss of Ift88 results in the absence of cilia and causes left-right asymmetry defects, disordered Hedgehog signaling, and polycystic kidney disease, all of which are explained by aberrant ciliary function. In addition, a number of extraciliary functions of Ift88 have been described that affect the cell-cycle, mitosis, and targeting of the T-cell receptor to the immunological synapse. Similarly, another essential ciliary molecule, the kinesin-2 subunit Kif3a, which transports Ift-B in the cilium, affects microtubule (MT) dynamics at the leading edge of migrating cells independently of cilia. We now show that loss of Ift88 impairs cell migration irrespective of cilia. Ift88 is required for the polarization of migrating MDCK cells, and Ift88 depleted cells have fewer MTs at the leading edge. Neither MT dynamics nor MT nucleation are dependent on Ift88. Our findings dissociate the function of Ift88 from Kif3a outside the cilium and suggest a novel extraciliary function for Ift88. Future studies need to address what unifying mechanism underlies the different extraciliary functions of Ift88.
doi_str_mv 10.1371/journal.pone.0140378
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subjects Animals
Antibiotics
Carrier Proteins - metabolism
Cell adhesion & migration
Cell cycle
Cell division
Cell migration
Cell Movement
Cell Polarity
Cilia
Dogs
Experiments
Fibroblasts
Flagella
Flagella - metabolism
Hedgehog protein
Immunological synapses
Immunology
Kidney diseases
Kidneys
Kinesin
Kinesin - metabolism
Lymphocytes T
Madin Darby Canine Kidney Cells
Mitosis
Nephrology
Polycystic kidney
Proteins
Signal transduction
Synapses
T cell receptors
T cells
T-cell receptor
Wound healing
title A Cilia Independent Role of Ift88/Polaris during Cell Migration
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