Journal
MOLECULAR BIOLOGY OF THE CELL
Volume 21, Issue 1, Pages 50-62Publisher
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E09-01-0089
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Funding
- Ludwig Institute for Cancer Research
- University of California, San Diego [T32 GM008666]
- National Cancer Institute
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM007752, T32GM008666] Funding Source: NIH RePORTER
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Signaling by the centrosomal asters and spindle midzone coordinately directs formation of the cytokinetic furrow. Here, we explore the contribution of the asters by analyzing the consequences of altering interaster distance during the first cytokinesis of the Caenorhabditis elegans embryo. Delaying aster separation, by using TPXL-1 depletion to shorten the metaphase spindle, leads to a corresponding delay in furrow formation, but results in a single furrow that ingresses at a normal rate. Preventing aster separation, by simultaneously inhibiting TPXL-1 and G alpha signaling-based cortical forces pulling on the asters, delays furrow formation and leads to the formation of multiple furrows that ingress toward the midzone. Disrupting midzone-based signaling, by depleting conserved midzone complexes, results in a converse phenotype: neither the timing nor the number of furrows is affected, but the rate of furrow ingression is decreased threefold. Simultaneously delaying aster separation and disrupting midzone-based signaling leads to complete failure of furrow formation. Based on these results, we propose that signaling by the separated asters executes two critical functions: 1) it couples furrow formation to anaphase onset by concentrating contractile ring proteins on the equatorial cortex in a midzone-independent manner and 2) it subsequently refines spindle midzone-based signaling to restrict furrowing to a single site.
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