Mis-specified cells die by an active gene-directed process, and inhibition of this death results in cell fate transformation in Drosophila

• Published in: Development (Cambridge) Vol. 132; no. 24; pp. 5343 - 5352
• Main Authors: Werz, Christian, Lee, Tom V, Lee, Peter L, Lackey, Melinda, Bolduc, Clare, Stein, David S, Bergmann, Andreas
• Format: Journal Article
• Language: English
• Published: England The Company of Biologists Limited 01.12.2005
• Subjects: Animals; Body Patterning; Caspases - metabolism; Cell Death - physiology; Cell Differentiation - physiology; Cell Survival; Drosophila; Drosophila - embryology; Drosophila - genetics; Drosophila - physiology; Drosophila Proteins - biosynthesis; Drosophila Proteins - genetics; Drosophila Proteins - physiology; Embryo, Nonmammalian - cytology; Embryo, Nonmammalian - physiology; Enzyme Activation; Gene Expression Regulation, Developmental; Homeodomain Proteins - genetics; Homeodomain Proteins - physiology; Mutation; Neuropeptides - biosynthesis; Neuropeptides - genetics; Neuropeptides - physiology; Receptor Protein-Tyrosine Kinases - genetics; Receptor Protein-Tyrosine Kinases - physiology; Signal Transduction; Trans-Activators - genetics; Trans-Activators - physiology
• ISSN: 0950-1991; 1477-9129
• DOI: 10.1242/dev.02150

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.