Format

Send to

Choose Destination
PLoS One. 2015 Oct 14;10(10):e0140378. doi: 10.1371/journal.pone.0140378. eCollection 2015.

A Cilia Independent Role of Ift88/Polaris during Cell Migration.

Author information

1
Department of Nephrology, University Hospital, Freiburg, Germany.
2
Life Imaging Center, Center for Biosystems Analysis, Albert-Ludwig-University, Freiburg, Germany; Center for Biological Signaling Studies (bioss), Albert-Ludwig-University, Freiburg, Germany.
3
Department of Nephrology, University Hospital, Freiburg, Germany; Center for Biological Signaling Studies (bioss), Albert-Ludwig-University, Freiburg, Germany.

Abstract

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.

PMID:
26465598
PMCID:
PMC4605505
DOI:
10.1371/journal.pone.0140378
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center