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Edits/additions for Asymmetric Cell Division > In Drosophila neural development

"Two proteins play an important role in setting up this [cell fate] asymmetry in the neuroblast, [:] Prospero and Numb."

In addition to the two daughter cells having separate fates, they have different cell sizes; the resulting neuroblast is much larger than the GMC. However, unlike with the proper segregation of fate determinants, asymmetric cell division that gives rise to cell size asymmetry is spindle-independent. The mechanism instead relies on the spatial and temporal organization of myosin on the cell cortex and its upstream components. Apical localization of Pins (Partner of Inscuteable) by Inscuteable allows Pins-dependent apical Protein Kinase N (Pkn) localization during metaphase. Pkn inhibits Rho-kinase (Rok), resulting in the timely loss of myosin and Rok from the apical cortex at anaphase onset. The apical myosin flows basally to where the cleavage furrow is positioned. Subsequently, the proteins Tum and Pav at the central spindle recruit myosin to increase myosin concentration, generating a myosin gradient to drive apical myosin flow from the basal cortex. This spatiotemporal control of myosin localization results in the asymmetric loss of cortical tension that normally pushes against hydrostatic pressure. In other words, the loss of apical cortical myosin allows hydrostatic pressure to push against the apical cell membrane, increasing the size of the apical region that is bound to become the larger neuroblast after cell division. Generation of apical and basal myosin flows simultaneously results in symmetric cell division, and delaying of basal myosin flows prevents normal expansion of the basal region of the dividing cell. Although this mechanism is spindle-independent, the spindle is important for setting up the cleavage furrow position, for bringing myosin to the cleavage furrow, and for driving basal myosin clearing.