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First published online January 10, 2008
doi: 10.1242/10.1242/jcs.015966

Journal of Cell Science 121, 155-161 (2008)
Published by The Company of Biologists 2008
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Short Report

Src and Wnt signaling regulate dynactin accumulation to the P2-EMS cell border in C. elegans embryos

Haining Zhang1,2, Ahna R. Skop1 and John G. White2,3,*

1 Laboratory of Genetics
2 Laboratory of Molecular Biology
3 Department of Anatomy, University of Wisconsin, Madison, WI 53706, USA

* Author for correspondence (e-mail: jwhite1{at}wisc.edu)

Accepted 22 October 2007

Summary

In many organisms, the dynein-dynactin complex is required for the alignment of the mitotic spindle onto the axis of polarity of a cell undergoing asymmetric cell division. How this complex transduces polarity cues, either intrinsic or extrinsic, and rotationally aligns the spindle accordingly is not well understood. The Caenorhabditis elegans blastomere P2 polarizes the neighboring EMS blastomere, which causes the EMS spindle to rotationally align along the defined axis of polarity via two redundant signaling pathways: Wnt and Src. Here, we describe how components of the dynactin complex became locally enriched at the P2-EMS border prior to and during rotational alignment of their spindles. Wnt and Src signaling were required for both localized dynactin enrichment, and for rotational alignment of the P2 and EMS spindles. Depleting the trimeric G-protein subunit G{alpha} did not abolish dynactin accumulation to the P2-EMS border, yet both EMS and P2 spindles failed to rotationally align, indicating that G{alpha} might act to regulate dynein/dynactin motor activity. By RNAi of a weak dnc-1(ts) allele, we showed that dynactin activity was required at least for EMS spindle rotational alignment.

Key words: Src and Wnt signaling, Dynactin, Enrichment, P2-EMS border


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JCS 2008 121: 201. [Full Text]  



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H. Zhang, A. R. Skop, and J. G. White
Src and Wnt signaling regulate dynactin accumulation to the P2-EMS cell border in C. elegans embryos
Development, February 1, 2008; 135(3): e1 - e1.
[Full Text]


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