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First published online 9 November 2005
doi: 10.1242/dev.02150

Development 132, 5343-5352 (2005)
Published by The Company of Biologists 2005
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Mis-specified cells die by an active gene-directed process, and inhibition of this death results in cell fate transformation in Drosophila

Christian Werz1,*, Tom V. Lee1,2, Peter L. Lee1, Melinda Lackey1, Clare Bolduc1, David S. Stein3 and Andreas Bergmann1,2,{dagger}

1 The University of Texas M.D. Anderson Cancer Center, Department of Biochemistry and Molecular Biology, 1515 Holcombe Boulevard, Unit 1000, Houston, TX 77030, USA
2 The Genes and Development Graduate Program (http://www.mdanderson.org/genedev)
3 The University of Texas at Austin, Patterson labs 532, Section of Molecular Cell and Developmental Biology, Institute for Cellular and Molecular Biology, 2401 W24th and Speedway, Austin, TX 78712, USA

{dagger} Author for correspondence (e-mail: abergman{at}mdanderson.org)

Accepted 5 October 2005

Incorrectly specified or mis-specified cells often undergo cell death or are transformed to adopt a different cell fate during development. The underlying cause for this distinction is largely unknown. In many developmental mutants in Drosophila, large numbers of mis-specified cells die synchronously, providing a convenient model for analysis of this phenomenon. The maternal mutant bicoid is particularly useful model with which to address this issue because its mutant phenotype is a combination of both transformation of tissue (acron to telson) and cell death in the presumptive head and thorax regions. We show that a subset of these mis-specified cells die through an active gene-directed process involving transcriptional upregulation of the cell death inducer hid. Upregulation of hid also occurs in oskar mutants and other segmentation mutants. In hid bicoid double mutants, mis-specified cells in the presumptive head and thorax survive and continue to develop, but they are transformed to adopt a different cell fate. We provide evidence that the terminal torso signaling pathway protects the mis-specified telson tissue in bicoid mutants from hid-induced cell death, whereas mis-specified cells in the head and thorax die, presumably because equivalent survival signals are lacking. These data support a model whereby mis-specification can be tolerated if a survival pathway is provided, resulting in cellular transformation.

Key words: Mis-specification, Cell death, Transformation, Bicoid, Oskar, Hid, Drosophila




This article has been cited by other articles:


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T. V. Lee, T. Ding, Z. Chen, V. Rajendran, H. Scherr, M. Lackey, C. Bolduc, and A. Bergmann
The E1 ubiquitin-activating enzyme Uba1 in Drosophila controls apoptosis autonomously and tissue growth non-autonomously
Development, January 1, 2008; 135(1): 43 - 52.
[Abstract] [Full Text] [PDF]


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