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Updated: Jul 20, 2026

A Cell-based Assay to Investigate Non-muscle Myosin II Contractility via the Folded-gastrulation Signaling Pathway in Drosophila S2R+ Cells
Published on: August 19, 2018
Control of G2/M transition by Drosophila Fos
Joogyung Hyun1, Isabelle Bécam, Constantin Yanicostas
1Department of Biomedical Genetics, University of Rochester Medical Center, Rochester, NY 14642, USA.
Abstract:
The transcription factors of the Fos family have long been associated with the control of cell proliferation, although the molecular and cellular mechanisms that mediate this function are poorly understood. We investigated the contributions of Fos to the cell cycle and cell growth control using Drosophila imaginal discs as a genetically accessible system. The RNA interference-mediated inhibition of Fos in proliferating cells of the wing and eye discs resulted in a specific defect in the G2-to-M-phase transition, while cell growth remained unimpaired, resulting in a marked reduction in organ size. Consistent with the conclusion that Fos is required for mitosis, we identified cyclin B as a direct transcriptional target of Fos in Drosophila melanogaster, with Fos binding to a region upstream of the cyclin B gene in vivo and cyclin B mRNA being specifically reduced under Fos loss-of-function conditions.
Insights
Fos transcription factors are crucial for cell cycle progression in Drosophila. Loss of Fos function specifically impairs the G2-to-M transition, impacting organ size by reducing mitosis.
Area of Science:
- Molecular Biology
- Developmental Biology
- Genetics
Background:
- Fos family transcription factors are linked to cell proliferation, but mechanisms remain unclear.
- Understanding Fos's role in cell cycle and growth control is essential.
Purpose of the Study:
- Investigate Fos's contribution to cell cycle and cell growth control.
- Elucidate the molecular mechanisms underlying Fos-mediated proliferation control.
Main Methods:
- Utilized Drosophila melanogaster imaginal discs as a model system.
- Employed RNA interference (RNAi) to inhibit Fos expression.
- Analyzed cell cycle progression and organ size defects.
- Identified direct transcriptional targets of Fos using in vivo binding assays.
Main Results:
- Fos inhibition caused a specific G2-to-M cell cycle transition defect.
- Cell growth was unaffected, but organ size was significantly reduced.
- Identified cyclin B as a direct transcriptional target of Fos.
- Fos binds upstream of the cyclin B gene, and its loss reduces cyclin B mRNA levels.
Conclusions:
- Fos is essential for regulating the G2-to-M cell cycle transition and mitosis.
- Fos controls organ size by regulating cyclin B expression.
- This study clarifies a key mechanism by which Fos family proteins regulate cell proliferation.
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