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Published online September 24, 2007
doi:10.1083/jcb.200703159
The Journal of Cell Biology, Vol. 178, No. 7, 1177-1191
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Goulding et al.
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Article

 Control of nuclear centration in the C. elegans zygote by receptor-independent G{alpha} signaling and myosin II

Morgan B. Goulding1, Julie C. Canman1, Eric N. Senning1,2, Andrew H. Marcus1,2, and Bruce Bowerman1

1 Institute of Molecular Biology and 2 Department of Chemistry, University of Oregon, Eugene, OR 97403

Correspondence to Morgan B. Goulding: goulding{at}uoregon.edu

Mitotic spindle positioning in the Caenorhabditis elegans zygote involves microtubule-dependent pulling forces applied to centrosomes. In this study, we investigate the role of actomyosin in centration, the movement of the nucleus–centrosome complex (NCC) to the cell center. We find that the rate of wild-type centration depends equally on the nonmuscle myosin II NMY-2 and the G{alpha} proteins GOA-1/GPA-16. In centration- defective let-99(–) mutant zygotes, GOA-1/GPA-16 and NMY-2 act abnormally to oppose centration. This suggests that LET-99 determines the direction of a force on the NCC that is promoted by G{alpha} signaling and actomyosin. During wild-type centration, NMY-2–GFP aggregates anterior to the NCC tend to move further anterior, suggesting that actomyosin contraction could pull the NCC. In GOA-1/GPA-16–depleted zygotes, NMY-2 aggregate displacement is reduced and largely randomized, whereas in a let-99(–) mutant, NMY-2 aggregates tend to make large posterior displacements. These results suggest that G{alpha} signaling and LET-99 control centration by regulating polarized actomyosin contraction.

Abbreviations used in this paper: AP, anteroposterior; DIC, differential interference contrast; EL, egg length; F-actin; filamentous actin; MSD, mean-squared displacement; MT, microtubule; NCC, nucleus–centrosome complex; NEB, nuclear envelope breakdown.


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