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Published on: January 12, 2020
Notch and Prospero repress proliferation following cyclin E overexpression in the Drosophila bristle lineage
Françoise Simon1, Pierre Fichelson, Michel Gho
1Université Pierre et Marie Curie-Paris 6, UMR 7622, Paris, France.
Abstract:
Understanding the mechanisms that coordinate cell proliferation, cell cycle arrest, and cell differentiation is essential to address the problem of how "normal" versus pathological developmental processes take place. In the bristle lineage of the adult fly, we have tested the capacity of post-mitotic cells to re-enter the cell cycle in response to the overexpression of cyclin E. We show that only terminal cells in which the identity is independent of Notch pathway undergo extra divisions after CycE overexpression. Our analysis shows that the responsiveness of cells to forced proliferation depends on both Prospero, a fate determinant, and on the level of Notch pathway activity. Our results demonstrate that the terminal quiescent state and differentiation are regulated by two parallel mechanisms acting simultaneously on fate acquisition and cell cycle progression.
Insights
Post-mitotic cells in adult flies can re-enter the cell cycle when cyclin E is overexpressed. Cell cycle re-entry depends on cell identity, specifically Notch pathway activity and Prospero, regulating differentiation.
Area of Science:
- Developmental Biology
- Cell Cycle Regulation
- Drosophila melanogaster research
Background:
- Coordinating cell proliferation, arrest, and differentiation is key to understanding normal and pathological development.
- The adult fly bristle lineage provides a model to study cell cycle control in post-mitotic cells.
Purpose of the Study:
- To investigate the capacity of post-mitotic cells to re-enter the cell cycle.
- To determine the factors influencing cell cycle re-entry upon cyclin E overexpression.
Main Methods:
- Overexpression of cyclin E in the adult fly bristle lineage.
- Analysis of cell division and differentiation markers.
- Assessing the role of Notch pathway activity and Prospero.
Main Results:
- Terminal cells independent of the Notch pathway divided upon cyclin E overexpression.
- Cellular responsiveness to forced proliferation is modulated by Prospero and Notch pathway activity.
- Two parallel mechanisms regulate terminal quiescence, differentiation, fate acquisition, and cell cycle progression.
Conclusions:
- Cellular fate and cell cycle progression are regulated by parallel mechanisms.
- Notch pathway activity and Prospero are critical regulators of cell cycle re-entry in differentiating cells.
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