In many systems, neural progenitor cells divide asymmetrically to generate a self-renewing progenitor and a committed neuron. How is this fate segregation controlled, and what defines the balance of proliferation and differentiation? Using live imaging in the developing zebrafish retina, Lucia Poggi and colleagues (p. 832) address these questions, focussing on the role of Anillin – a protein involved in cytokinesis – in the cell divisions that generate retinal ganglion cells (RGCs). By following individual divisions, the authors find that Anillin is itself asymmetrically inherited between daughter cells, and directs the asymmetric inheritance of actin and the polarity protein Par3. Cells with reduced Anillin levels tend to divide symmetrically, generating two RGCs rather than a progenitor and a RGC. Globally, this results in a retina with more RGCs. The authors further show that anillin expression is itself regulated by the RGC fate determinant Ath5, suggesting that there may be feedback loops involving Ath5 and Anillin that control the balance of proliferation and differentiation. How Anillin acts to regulate asymmetric division and fate choice remains unclear, but this technically challenging study demonstrates the importance of this protein in the control of neurogenesis in the retina.
Asymmetric division and fate in the retina
Asymmetric division and fate in the retina. Development 1 March 2015; 142 (5): e0505. doi:
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