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Published online January 21, 2008
doi:10.1083/jcb.200708159
The Journal of Cell Biology, Vol. 180, No. 2, 267-272
The Rockefeller University Press, 0021-9525 $30.00
© 2008 Chia et al.
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 Drosophila neuroblast asymmetric divisions: cell cycle regulators, asymmetric protein localization, and tumorigenesis

William Chia1,2, W. Gregory Somers1, and Hongyan Wang3

1 Temasek Life Sciences Laboratory and 2 Department of Biological Sciences, National University of Singapore, Singapore 1176043 Duke-NUS Graduate Medical School, Singapore 169547

Correspondence to William Chia: wchia{at}tll.org.sg

Over the past decade, many of the key components of the genetic machinery that regulate the asymmetric division of Drosophila melanogaster neural progenitors, neuroblasts, have been identified and their functions elucidated. Studies over the past two years have shown that many of these identified components act to regulate the self-renewal versus differentiation decision and appear to function as tumor suppressors during larval nervous system development. In this paper, we highlight the growing number of molecules that are normally considered to be key regulators of cell cycle events/progression that have recently been shown to impinge on the neuroblast asymmetric division machinery to control asymmetric protein localization and/or the decision to self-renew or differentiate.

Abbreviations used in this paper: APC/C, anaphase-promoting complex/cyclosome; aPKC, atypical PKC; GMC, ganglion mother cell.


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