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Dev Cell. 2010 Nov 16;19(5):778-85. doi: 10.1016/j.devcel.2010.10.007.

Interplay between the transcription factor Zif and aPKC regulates neuroblast polarity and self-renewal.

Author information

1
Temasek Life Sciences Laboratory, 1 Research Link, Singapore 117604.

Abstract

How a cell decides to self-renew or differentiate is a critical issue in stem cell and cancer biology. Atypical protein kinase C (aPKC) promotes self-renewal of Drosophila larval brain neural stem cells, neuroblasts. However, it is unclear how aPKC cortical polarity and protein levels are regulated. Here, we have identified a zinc-finger protein, Zif, which is required for the expression and asymmetric localization of aPKC. aPKC displays ectopic cortical localization with upregulated protein levels in dividing zif mutant neuroblasts, leading to neuroblast overproliferation. We show that Zif is a transcription factor that directly represses aPKC transcription. We further show that Zif is phosphorylated by aPKC both in vitro and in vivo. Phosphorylation of Zif by aPKC excludes it from the nucleus, leading to Zif inactivation in neuroblasts. Thus, reciprocal repression between Zif and aPKC act as a critical regulatory mechanism for establishing cell polarity and controlling neuroblast self-renewal.

PMID:
21074726
DOI:
10.1016/j.devcel.2010.10.007
[Indexed for MEDLINE]
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