期刊
JOURNAL OF CELL BIOLOGY
卷 178, 期 7, 页码 1177-1191出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200703159
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- NIGMS NIH HHS [R01GM67891, R01 GM049869, R01 GM067891, R01GM49869] Funding Source: Medline
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 Ga signaling and LET-99 control centration by regulating polarized actomyosin contraction.
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