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Notch signaling through tramtrack bypasses the mitosis promoting activity of the JNK pathway in the mitotic-to-endocycle transition of Drosophila follicle cells
Journal article   Open access   Peer reviewed

Notch signaling through tramtrack bypasses the mitosis promoting activity of the JNK pathway in the mitotic-to-endocycle transition of Drosophila follicle cells

Katherine C Jordan, Valerie Schaeffer, Karin A Fischer, Elizabeth E Gray and Hannele Ruohola-Baker
BMC developmental biology, v 6(1), pp 16-16
16 Mar 2006
PMID: 16542414
url
https://bmcdevbiol.biomedcentral.com/track/pdf/10.1186/1471-213X-6-16View
Published, Version of Record (VoR) Open
url
https://doi.org/10.1186/1471-213X-6-16View
Published, Version of Record (VoR) Open

Abstract

Animals Cell Differentiation Drosophila melanogaster - cytology Drosophila melanogaster - enzymology Drosophila melanogaster - physiology Drosophila Proteins - metabolism Epithelial Cells - metabolism Female JNK Mitogen-Activated Protein Kinases - metabolism Mitosis - physiology Models, Biological Molecular Mimicry Ovarian Follicle - cytology Ovarian Follicle - metabolism Receptors, Notch - metabolism Repressor Proteins - metabolism Signal Transduction
The follicle cells of the Drosophila egg chamber provide an excellent model in which to study modulation of the cell cycle. During mid-oogenesis, the follicle cells undergo a variation of the cell cycle, endocycle, in which the cells replicate their DNA, but do not go through mitosis. Previously, we showed that Notch signaling is required for the mitotic-to-endocycle transition, through downregulating String/Cdc25, and Dacapo/p21 and upregulating Fizzy-related/Cdh1. In this paper, we show that Notch signaling is modulated by Shaggy and temporally induced by the ligand Delta, at the mitotic-to-endocycle transition. In addition, a downstream target of Notch, tramtrack, acts at the mitotic-to-endocycle transition. We also demonstrate that the JNK pathway is required to promote mitosis prior to the transition, independent of the cell cycle components acted on by the Notch pathway. This work reveals new insights into the regulation of Notch-dependent mitotic-to-endocycle switch.

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