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Updated: Oct 6, 2026
Dissection and Immunostaining of Imaginal Discs from Drosophila melanogaster
Published on: September 19, 2014
Bar represses dPax2 and decapentaplegic to regulate cell fate and morphogenetic cell death in Drosophila eye
Jongkyun Kang1, Eunbyul Yeom1, Janghoo Lim2
1Department of Biological Sciences, Korea Advanced Institute of Science & Technology, Daejeon, Korea.
Abstract:
The coordinated regulation of cell fate and cell survival is crucial for normal pattern formation in developing organisms. In Drosophila compound eye development, crystalline arrays of hexagonal ommatidia are established by precise assembly of diverse cell types, including the photoreceptor cells, cone cells and interommatidial (IOM) pigment cells. The molecular basis for controlling the number of cone and IOM pigment cells during ommatidial pattern formation is not well understood. Here we present evidence that BarH1 and BarH2 homeobox genes are essential for eye patterning by inhibiting excess cone cell differentiation and promoting programmed death of IOM cells. Specifically, we show that loss of Bar from the undifferentiated retinal precursor cells leads to ectopic expression of Prospero and dPax2, two transcription factors essential for cone cell specification, resulting in excess cone cell differentiation. We also show that loss of Bar causes ectopic expression of the TGFβ homolog Decapentaplegic (Dpp) posterior to the morphogenetic furrow in the larval eye imaginal disc. The ectopic Dpp expression is not responsible for the formation of excess cone cells in Bar loss-of-function mutant eyes. Instead, it causes reduction in IOM cell death in the pupal stage by antagonizing the function of pro-apoptotic gene reaper. Taken together, this study suggests a novel regulatory mechanism in the control of developmental cell death in which the repression of Dpp by Bar in larval eye disc is essential for IOM cell death in pupal retina.
Insights
Bar homeobox genes regulate Drosophila eye development by controlling cell numbers. Loss of Bar leads to excess cone cells and reduced pigment cell death, revealing a novel developmental cell death mechanism.
Area of Science:
- Developmental Biology
- Genetics
- Cell Biology
Background:
- Coordinated regulation of cell fate and survival is vital for pattern formation.
- Drosophila compound eye development involves precise assembly of photoreceptor, cone, and interommatidial (IOM) pigment cells.
- Molecular mechanisms controlling cone and IOM cell numbers during ommatogenesis are poorly understood.
Purpose of the Study:
- Investigate the role of BarH1 and BarH2 homeobox genes in Drosophila eye patterning.
- Elucidate the molecular basis for controlling cone and IOM cell populations.
- Understand the regulation of developmental cell death in the eye imaginal disc.
Main Methods:
- Analysis of Bar loss-of-function mutants in Drosophila eye imaginal discs.
- Examination of gene expression patterns, including Prospero, dPax2, and Decapentaplegic (Dpp).
- Assessment of cell differentiation and programmed cell death during eye development.
Main Results:
- Loss of Bar function in retinal precursor cells causes excess cone cell differentiation due to ectopic Prospero and dPax2 expression.
- Bar deficiency leads to ectopic Decapentaplegic (Dpp) expression posterior to the morphogenetic furrow.
- Ectopic Dpp antagonizes reaper, a pro-apoptotic gene, resulting in reduced IOM cell death in pupal stages.
Conclusions:
- Bar homeobox genes are essential for inhibiting excess cone cell differentiation.
- Bar genes promote IOM cell programmed death by repressing Dpp signaling.
- Repression of Dpp by Bar in the larval eye disc is critical for regulating IOM cell death in the pupal retina, establishing a novel developmental cell death regulatory mechanism.
