1. Howard Hughes Medical Institute and Departments of Physiology and Biochemistry, University of California at San Francisco, San Francisco , California 94143-0725, USA

Correspondence to: Yuh Nung Jan Correspondence and requests for materials should be addressed to Y.N.J. (e-mail: Email: ynjan@itsa.ucsf.edu).

Abstract

Asymmetric division is a fundamental mechanism for generating cellular diversity. In the central nervous system of Drosophila, neural progenitor cells called neuroblasts undergo asymmetric division along the apical–basal cellular axis^{1, 2}. Neuroblasts originate from neuroepithelial cells, which are polarized along the apical–basal axis and divide symmetrically along the planar axis. The asymmetry of neuroblasts might arise from neuroblast-specific expression of the proteins required for asymmetric division. Alternatively, both neuroblasts and neuroepithelial cells could be capable of dividing asymmetrically, but in neuroepithelial cells other polarity cues might prevent asymmetric division. Here we show that by disrupting adherens junctions we can convert the symmetric epithelial division into asymmetric division. We further confirm that the adenomatous polyposis coli (APC) tumour suppressor protein is recruited to adherens junctions³, and demonstrate that both APC and microtubule-associated EB1 homologues^{3, 4, 5} are required for the symmetric epithelial division along the planar axis. Our results indicate that neuroepithelial cells have all the necessary components to execute asymmetric division, but that this pathway is normally overridden by the planar polarity cue provided by adherens junctions.