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Updated: Jun 26, 2026
In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila
Published on: November 27, 2016
Regulation of apoptosis of rbf mutant cells during Drosophila development
Miho Tanaka-Matakatsu1, Jinhua Xu, Leping Cheng
1Ben May Department for Cancer Research, the University of Chicago, Chicago, IL 60637, USA.
Abstract:
Inactivation of the retinoblastoma gene Rb leads to defects in cell proliferation, differentiation, or apoptosis, depending on specific cell or tissue types. To gain insights into the genes that can modulate the consequences of Rb inactivation, we carried out a genetic screen in Drosophila to identify mutations that affected apoptosis induced by inactivation of the Retinoblastoma-family protein (rbf) and identified a mutation that blocked apoptosis induced by rbf. We found this mutation to be a new allele of head involution defective (hid) and showed that hid expression is deregulated in rbf mutant cells in larval imaginal discs. We identified an enhancer that regulates hid expression in response to developmental cues as well as to radiation and demonstrated that this hid enhancer is directly repressed by RBF through an E2F binding site. These observations indicate that apoptosis of rbf mutant cells is mediated by an upregulation of hid. Finally, we showed that bantam, a miRNA that regulates hid translation, is expressed in the interommatidial cells in the larval eye discs and modulates the survival of rbf mutant cells.
Insights
Inactivating the retinoblastoma gene (Rb) causes cell defects. We found that the head involution defective (hid) gene blocks apoptosis in Rb-mutant cells by upregulating hid expression.
Area of Science:
- Cell Biology
- Genetics
- Developmental Biology
Background:
- Inactivation of the retinoblastoma gene (Rb) impacts cell proliferation, differentiation, and apoptosis.
- Understanding genes that modulate Rb inactivation consequences is crucial for cell fate determination.
Purpose of the Study:
- To identify genes modulating apoptosis induced by Retinoblastoma-family protein (rbf) inactivation in Drosophila.
- To elucidate the regulatory mechanisms of apoptosis following rbf loss.
Main Methods:
- Conducted a genetic screen in Drosophila to identify mutations affecting rbf-induced apoptosis.
- Utilized larval imaginal discs and eye discs for molecular and genetic analyses.
- Investigated gene expression, enhancer activity, and microRNA regulation.
Main Results:
- Identified a novel allele of head involution defective (hid) that blocks apoptosis in rbf mutant cells.
- Demonstrated deregulated hid expression in rbf mutant cells, mediated by RBF-repressed E2F binding site.
- Showed that bantam microRNA modulates the survival of rbf mutant cells by regulating hid translation.
Conclusions:
- Apoptosis of rbf mutant cells is primarily mediated by the upregulation of hid.
- RBF directly represses a hid enhancer, linking Rb pathway to apoptosis regulation.
- Bantam microRNA plays a role in controlling cell survival in the context of Rb inactivation.
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