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Updated: Aug 26, 2026
Imaging Dpp Release from a Drosophila Wing Disc
Published on: October 30, 2019
Repression of dMyc expression by Wingless promotes Rbf-induced G1 arrest in the presumptive Drosophila wing margin
Molly Duman-Scheel1, Laura A Johnston, Wei Du
1Ben May Institute for Cancer Research and Center for Molecular Oncology, University of Chicago, 924 East 57th Street, Chicago, IL 60637, USA.
Abstract:
Little is known about how patterns of cell proliferation and arrest are generated during development, a time when tight regulation of the cell cycle is necessary. In this study, the mechanism by which the developmental signaling molecule Wingless (Wg) generates G(1) arrest in the presumptive Drosophila wing margin is examined in detail. Wg signaling promotes activity of the Drosophila retinoblastoma family (Rbf) protein, which is required for G(1) arrest in the presumptive wing margin. Wg promotes Rbf function by repressing expression of the G(1)-S regulator Drosophila myc (dmyc). Ectopic expression of dMyc induces expression of Cyclin E, Cyclin D, and Cdk4, which can inhibit Rbf and promote G(1)-S progression. Thus, G(1) arrest in the presumptive wing margin depends on the presence of Rbf, which is maintained by the ability of Wg signaling to repress dmyc expression in these cells. In addition to advancing the understanding of how patterned cell-cycle arrest is generated by the Wg signaling molecule during development, this study indicates that components of the Rbf/E2f pathway are targets of dMyc in Drosophila. Although Rbf/E2f pathway components mediate the ability of dMyc to promote G(1) progression, dMyc appears to regulate growth independently of the RBF/E2f pathway.
Insights
Wingless (Wg) signaling in Drosophila development establishes cell cycle arrest by promoting the retinoblastoma protein (Rbf) and repressing Drosophila myc (dmyc). This Wg-Rbf-dmyc pathway is crucial for patterned G(1) arrest.
Area of Science:
- Developmental Biology
- Cell Cycle Regulation
- Molecular Genetics
Background:
- Cell cycle control is critical during development, yet mechanisms generating patterned cell proliferation and arrest remain incompletely understood.
- The developmental signaling molecule Wingless (Wg) plays a key role in orchestrating developmental processes, including cell fate determination and tissue patterning.
Purpose of the Study:
- To elucidate the molecular mechanism by which Wingless (Wg) signaling induces G(1) cell cycle arrest in the presumptive Drosophila wing margin.
- To investigate the interplay between Wg signaling, the retinoblastoma protein (Rbf), and Drosophila myc (dmyc) in regulating cell proliferation during development.
Main Methods:
- Detailed examination of the Wg signaling pathway in the Drosophila wing margin.
- Analysis of gene expression patterns, including Rbf, dmyc, Cyclin E, Cyclin D, and Cdk4.
- Experimental manipulation of dMyc expression to assess its impact on cell cycle progression and Rbf activity.
Main Results:
- Wg signaling promotes G(1) arrest by enhancing the activity of the Drosophila retinoblastoma protein (Rbf).
- Wg signaling achieves this by repressing the expression of Drosophila myc (dmyc), a G(1)-S phase regulator.
- Ectopic expression of dMyc leads to increased Cyclin E, Cyclin D, and Cdk4, which can overcome Rbf-mediated inhibition and drive G(1)-S progression.
- Components of the Rbf/E2f pathway are identified as targets of dMyc, mediating dMyc's promotion of G(1) progression.
Conclusions:
- G(1) arrest in the presumptive Drosophila wing margin is dependent on Rbf, whose function is maintained by Wg-mediated repression of dmyc.
- Wg signaling provides a critical mechanism for generating patterned cell-cycle arrest during development.
- dMyc regulates growth independently of the Rbf/E2f pathway, despite Rbf/E2f pathway components being targets of dMyc.
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