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First published online 22 February 2006
doi: 10.1242/dev.02299

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Steroid hormone-dependent transformation of polyhomeotic mutant neurons in the Drosophila brain

Jian Wang^1,*, Ching-Hsien J. Lee^2,*, Suewei Lin³ and Tzumin Lee^3,

¹ Department of Entomology, University of Maryland, College Park, MD 20742, USA.
² Division of Hematology Oncology, Department of Medicine, University of Massachusetts Memorial Medical Center, Worcester, MA 01655, USA.
³ Department of Neurobiology, University of Massachusetts Medical School, Worcester, MA 01605, USA.

Author for correspondence (e-mail: tzumin.lee{at}umassmed.edu)

Accepted 24 January 2006

Polyhomeotic (Ph), which forms complexes with other Polycomb-group (PcG) proteins, is widely required for maintenance of cell identity by ensuring differential gene expression patterns in distinct types of cells. Genetic mosaic screens in adult fly brains allow for recovery of a mutation that simultaneously disrupts the tandemly duplicated Drosophila ph transcriptional units. Distinct clones of neurons normally acquire different characteristic projection patterns and can be differentially labeled using various subtype-specific drivers in mosaic brains. Such neuronal diversity is lost without Ph. In response to ecdysone, ph mutant neurons are transformed into cells with unidentifiable projection patterns and indistinguishable gene expression profiles during early metamorphosis. Some subtype-specific neuronal drivers become constitutively activated, while others are constantly suppressed. By contrast, loss of other PcG proteins, including Pc and E(z), causes different neuronal developmental defects; and, consistent with these phenomena, distinct Hox genes are differentially misexpressed in different PcG mutant clones. Taken together, Drosophila Ph is essential for governing neuronal diversity, especially during steroid hormone signaling.

Key words: Polyhomeotic, Polycomb group, Neuronal cell fate maintenance, Ecdysone, Metamorphosis

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Polyhomeotic: a neuronal memory aid?

Development 2006 133: e701. [Full Text]  

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