Abstract
Precise cleavage furrow positioning is required for faithful chromosome segregation and cell fate determinant distribution. In most metazoan cells, contractile ring placement is regulated by the mitotic spindle through the centralspindlin complex, and potentially also the chromosomal passenger complex (CPC). Drosophila neuroblasts, asymmetrically dividing neural stem cells, but also other cells utilize both spindle-dependent and spindle-independent cleavage furrow positioning pathways. However, the relative contribution of each pathway towards cytokinesis is currently unclear. Here we report that in Drosophila neuroblasts, the mitotic spindle, but not polarity cues, controls the localization of the CPC component Survivin. We also show that Survivin and the mitotic spindle are required to stabilize the position of the cleavage furrow in late anaphase and to complete furrow constriction. These results support the model that two spatially and temporally separate pathways control different key aspects during asymmetric cell division, ensuring correct cell fate determinant segregation and neuroblast self-renewal.
Highlights
Precise cleavage furrow positioning is required for faithful chromosome segregation and cell fate determinant distribution
Current models propose that Pav/mitotic kinesinlike protein 1 (MKLP1) travels along stable cortical microtubules (MTs), delivering Tum to the cell equator where it activates the RhoGEF Pebble (Pbl in Drosophila; ECT2 in vertebrates and LET-21 in C. elegans)[6,7,8]
To understand the dynamic localization of the chromosomal passenger complex (CPC) during asymmetric cell division, we started our analysis with time lapse imaging experiments of the CPC component Survivin in Drosophila neuroblasts
Summary
Precise cleavage furrow positioning is required for faithful chromosome segregation and cell fate determinant distribution. We show that Survivin and the mitotic spindle are required to stabilize the position of the cleavage furrow in late anaphase and to complete furrow constriction These results support the model that two spatially and temporally separate pathways control different key aspects during asymmetric cell division, ensuring correct cell fate determinant segregation and neuroblast self-renewal. Genetic and chemical spindle ablation and rotation experiments demonstrated that this symmetry-breaking event is independent of MTs (spindle independent), but requires the polarity proteins Discs large 1 (Dlg1) and partner of inscuteable (Pins; AGS3/LGN in vertebrates; polarity dependent)[11,15] This asymmetric Myosin distribution allows for unequal cortical expansion, pushing the cleavage furrow towards the basal cortex[15], a mechanism that is conserved in the C. elegans Q-neuroblast lineage[12]. Whether this applies to the CPC remains to be tested
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