QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

First published online 7 February 2007
doi: 10.1242/dev.02793

This Article Figures Only Full Text Full Text (PDF) All Versions of this Article: dev.02793v1 134/6/1091    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Development Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bello, B. Articles by Reichert, H. Search for Related Content PubMed PubMed Citation Articles by Bello, B. Articles by Reichert, H.

Polycomb group genes are required for neural stem cell survival in postembryonic neurogenesis of Drosophila

Biozentrum, University of Basel, Klingelbergstrasse 50, CH-4056 Basel, Switzerland.

^* Author for correspondence (e-mail: Bruno.Bello{at}unibas.ch)

Accepted 28 December 2006

Genes of the Polycomb group (PcG) are part of a cellular memory system that maintains appropriate inactive states of Hox gene expression in Drosophila. Here, we investigate the role of PcG genes in postembryonic development of the Drosophila CNS. We use mosaic-based MARCM techniques to analyze the role of these genes in the persistent larval neuroblasts and progeny of the central brain and thoracic ganglia. We find that proliferation in postembryonic neuroblast clones is dramatically reduced in the absence of Polycomb, Sex combs extra, Sex combs on midleg, Enhancer of zeste or Suppressor of zeste 12. The proliferation defects in these PcG mutants are due to the loss of neuroblasts by apoptosis in the mutant clones. Mutation of PcG genes in postembryonic lineages results in the ectopic expression of posterior Hox genes, and experimentally induced misexpression of posterior Hox genes, which in the wild type causes neuroblast death, mimics the PcG loss-of-function phenotype. Significantly, full restoration of wild-type-like properties in the PcG mutant lineages is achieved by blocking apoptosis in the neuroblast clones. These findings indicate that loss of PcG genes leads to aberrant derepression of posterior Hox gene expression in postembryonic neuroblasts, which causes neuroblast death and termination of proliferation in the mutant clones. Our findings demonstrate that PcG genes are essential for normal neuroblast survival in the postembryonic CNS of Drosophila. Moreover, together with data on mammalian PcG genes, they imply that repression of aberrant reactivation of Hox genes may be a general and evolutionarily conserved role for PcG genes in CNS development.

Key words: Polycomb group, Drosophila, Neurogenesis, Hox genes, Neuroblasts

Related articles in Development:

A death sentence for neuroblasts

Development 2007 134: e602. [Full Text]  

This article has been cited by other articles:

				C. Q. Doe Neural stem cells: balancing self-renewal with differentiation Development, May 1, 2008; 135(9): 1575 - 1587. [Abstract] [Full Text] [PDF]

				M. E. Kaplow, A. H. Korayem, and T. R. Venkatesh Regulation of Glia Number in Drosophila by Rap/Fzr, an Activator of the Anaphase-Promoting Complex, and Loco, an RGS Protein Genetics, April 1, 2008; 178(4): 2003 - 2016. [Abstract] [Full Text] [PDF]