
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.
Receptors, Notch, Down-Regulation, Gene Expression, Nuclear Proteins, Cell Differentiation, Nerve Tissue Proteins, QH426-470, Cyclin E, Genetics, Animals, Drosophila Proteins, Cell Lineage, Drosophila, Research Article, Cell Proliferation, Transcription Factors
Receptors, Notch, Down-Regulation, Gene Expression, Nuclear Proteins, Cell Differentiation, Nerve Tissue Proteins, QH426-470, Cyclin E, Genetics, Animals, Drosophila Proteins, Cell Lineage, Drosophila, Research Article, Cell Proliferation, Transcription Factors
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