Asymmetric cortical extension shifts cleavage furrow position inDrosophilaneuroblasts

Abstract

A spindle-independent, myosin II–containing domain causes asymmetric cortical extension during anaphase of asymmetrically dividing Drosophila neuroblasts. Heterotrimeric G-proteins regulate the activity of the myosin II domain, and their loss leads to symmetric expansion and daughter cell size.

Coupling changes in cell shape to chromosome segregation

“…In previous decades, this type of activity was often attributed to the ability of the growing, plus ends of astral microtubules to induce cortical softening at cell poles 108 . Although the complex ity of microtubulebased signals are yet to be resolved (for example, furrow components accumulate at the tips of microtubules in the absence of micro tubule overlap in cells exiting mitosis with a monopolar spindle 109,110 ), it is now clear that the anaphase spindle 106,[111][112][113] also signals to the cortex via microtubuleindependent sig nals. In support of this, polar relaxation still occurs near anaphase chromatin in cells that lack spindle poles and/or microtubules 106 .…”

Stem Cells and Asymmetric Cell Division

“…Basal displacement of the cleavage furrow involves Pinsmediated localisation of proteins normally found associated with cleavage-furrows, including the homologue of Kinesin-like protein 23 (Pavarotti, in fl ies), the actinbinding protein Anillin (Scraps, in fl ies), and Myosin II heavy chain (Zipper, Zip, in fl ies) (Cabernard et al 2010 ). This so-called "basal furrow domain" has recently been shown to function in the asymmetric positioning of the cleavage furrow by inhibiting cortical extension specifi cally on the basal side (Connell et al 2011 ). Analogy has been drawn with the C. elegans zygote, whereby Myosin II polarisation could drive asymmetric cortical behaviour.…”

“…Analogy has been drawn with the C. elegans zygote, whereby Myosin II polarisation could drive asymmetric cortical behaviour. During neuroblast mitosis, Myosin II is enriched apically during prometaphase and on the basal cortex during anaphase (Barros et al 2003 ;Connell et al 2011 ). Here, it presumably exerts strongest force, which, along with lack of resistance from the opposite (apical) cortex, has been proposed to promote asymmetric cortical extension at anaphase, contributing to the size difference of resulting daughter cells (Connell et al 2011 ).…”

Control of asymmetric cell division

“…For instance, asymmetrically dividing Drosophila neuroblasts utilize the polarity proteins Discs large 1 (Dlg1) and Partner of Inscuteable (Pins; AGS3/LGN in vertebrates) to asymmetrically localize Myosin, positioning the cleavage furrow off-center [58,62].…”

“…Asymmetric Myosin distribution has been proposed to drive unequal cortical expansion, pushing the cleavage furrow off-center [61,62]. For instance, Myosin enrichment on one side of the cell could create higher active cortical tension while at the same time reducing cortical stiffness on the opposite cell pole.…”