Caenorhabditis elegans EFA-6 limits microtubule growth at the cell cortex

Abstract

EFA-6, originally identified as a suppressor of defects associated with dynein muations in early Caenorhabditis elegans embryos, regulates microtubule growth at the embryo cortex through a conserved amino-terminal motif but independently of its ARF6 GTP exchange factor activity. Microtubules are polymers of tubulin heterodimers that exhibit dynamic instability: periods of growth followed by periods of shrinkage1. However, the molecular regulation of dynamic instability remains elusive. Here, we show that EFA-6, a cortically-localized protein2, limits the growth of microtubules near the cell cortex of early embryonic cells from Caenorhabidits elegans, possibly by inducing microtubule catastrophes. Compared with wild type, embryos lacking EFA-6 had abnormally long and dense microtubules at the cell cortex, and growing microtubule plus ends resided at the cortex for up to five-fold longer. Loss of EFA-6 also caused excess centrosome separation and displacement towards the cell cortex early in mitosis, and subsequently a loss of anaphase spindle-pole oscillations and increased rates of spindle elongation. The centrosome separation phenotype was dependent on the motor protein dynein, suggesting a possible link between the modulation of microtubule dynamics at the cortex and dynein-dependent force production. EFA-6 orthologues activate ARF6-type GTPases to regulate vesicle trafficking3. However, we show that only the C. elegans EFA-6 amino-terminus is both necessary and sufficient to limit microtubule growth along the cortex, and that this function is independent of ARF-6.

Cite this article

O'Rourke, S., Christensen, S. & Bowerman, B. Caenorhabditis elegans EFA-6 limits microtubule growth at the cell cortex. Nat Cell Biol 12, 1235–1241 (2010). https://doi.org/10.1038/ncb2128

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