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Updated: Aug 19, 2026
Dissection and Immunostaining of Imaginal Discs from Drosophila melanogaster
Published on: September 20, 2014
Ectopic expression of dE2F and dDP induces cell proliferation and death in the Drosophila eye
Abstract:
The deregulation of E2F activity is thought to contribute to the uncontrolled proliferation of many tumor cells. While the effects of overexpressing E2F genes have been studied extensively in tissue culture, the consequences of elevating E2F activity in vivo are unknown. To address this issue, transgenic lines of Drosophila were studied in which ectopic expression of dE2F and dDP was targeted to the developing eye. The co-expression of dDP or dE2F disrupted normal eye development, resulting in abnormal patterns of bristles, cone cells and photoreceptors. dE2F/dDP expression caused ectopic S phases in post-mitotic cells of the eye imaginal disc but did not disrupt the onset of neuronal differentiation. Most S phases were seen in uncommitted cells, although some cells that had initiated photo-receptor differentiation were also driven into the cell cycle. Elevated expression of dE2F and dDP caused apoptosis in the eye disc. The co-expression of baculovirus p35 protein, an inhibitor of cell death, strongly enhanced the dE2F/dDP-dependent phenotype. These results show that, in this in vivo system, the elevation of E2F activity caused post-mitotic cells to enter the cell cycle. However, these cells failed to proliferate unless rescued from apoptosis.
Insights
Elevating E2F activity in Drosophila eyes forces post-mitotic cells into the cell cycle. However, these cells undergo apoptosis and fail to proliferate without rescue, revealing in vivo cell cycle control mechanisms.
Area of Science:
- Cell Biology
- Developmental Biology
- Genetics
Background:
- Deregulation of E2F activity is linked to tumor cell proliferation.
- In vivo consequences of elevated E2F activity remain largely unknown.
- Previous studies focused on E2F gene overexpression in tissue culture.
Purpose of the Study:
- To investigate the in vivo effects of elevated E2F activity on cell proliferation and differentiation.
- To understand the role of E2F in regulating cell cycle entry in post-mitotic cells.
- To explore the interplay between E2F activity, cell cycle progression, and apoptosis in a developing organism.
Main Methods:
- Generation of transgenic Drosophila with targeted ectopic expression of dE2F and dDP in the developing eye.
- Analysis of eye development, cell differentiation, and cell cycle progression (S phase) in transgenic flies.
- Assessment of apoptosis using co-expression of baculovirus p35 protein (an apoptosis inhibitor).
Main Results:
- Ectopic co-expression of dE2F and dDP disrupted normal eye development, affecting bristles, cone cells, and photoreceptors.
- Elevated E2F/dDP expression induced ectopic S phases in post-mitotic cells of the eye imaginal disc.
- While neuronal differentiation onset was not disrupted, some differentiating photoreceptor cells re-entered the cell cycle.
- Increased dE2F/dDP expression led to apoptosis, which was enhanced by p35 co-expression, suggesting rescued cells could proliferate.
Conclusions:
- Elevated E2F activity in vivo can drive post-mitotic cells into the cell cycle.
- Cell cycle re-entry does not guarantee proliferation; apoptosis is a critical barrier.
- The study highlights the complex regulation of cell proliferation and survival in vivo, influenced by E2F activity and apoptotic pathways.
