PLR-1, a putative E3 ubiquitin ligase, controls cell polarity and axonal extensions in C. elegans.

Autor: Bhat JM; Department of Biological Sciences, Simon Fraser University, Burnaby, BC, Canada V5A 1S6., Pan J; Department of Biological Sciences, Simon Fraser University, Burnaby, BC, Canada V5A 1S6., Hutter H; Department of Biological Sciences, Simon Fraser University, Burnaby, BC, Canada V5A 1S6. Electronic address: hutter@sfu.ca.
Jazyk: angličtina
Zdroj: Developmental biology [Dev Biol] 2015 Feb 01; Vol. 398 (1), pp. 44-56. Date of Electronic Publication: 2014 Nov 20.
DOI: 10.1016/j.ydbio.2014.11.008
Abstrakt: During embryonic development neurons differentiate and extend axons and dendrites that have to reach their appropriate targets. In Caenorhabditis elegans the AVG neuron is the first neuron to extend an axon during the establishment of the ventral nerve cord, the major longitudinal axon tract in the animal. In genetic screens we isolated alleles of plr-1, which caused polarity reversals of the AVG neuron as well as outgrowth and navigation defects of the AVG axon. In addition plr-1 mutants show outgrowth defects in several other classes of neurons as well as the posterior excretory canals. plr-1 is predicted to encode a transmembrane E3 ubiquitin ligase and is widely expressed in the animal including the AVG neuron and the excretory cell. plr-1 has recently been shown to negatively regulate Wnt signalling by removing Wnt receptors from the cell surface. We observed that mutations in a gene reducing Wnt signalling as well as mutations in unc-53/NAV2 and unc-73/Trio suppress the AVG polarity defects in plr-1 mutants, but not the defects seen in other cells. This places plr-1 in a Wnt regulation pathway, but also suggests that plr-1 has Wnt independent functions and interacts with unc-53 and unc-73 to control cell polarity.
(Copyright © 2014 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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