Notch-dependent downregulation of the homeodomain gene cut is required for the mitotic cycle/endocycle switch and cell differentiation in<i>Drosophila</i>follicle cells

Sun, Jianjun; Deng, Wu-Min

doi:10.1242/dev.02015

Cited by 134 publications

(203 citation statements)

References 57 publications

(68 reference statements)

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“…In the Drosophila ovary, it was first shown to be required for maintaining follicle cells in their precursor stage and for specification of polar cells that mark the ends of the egg chamber (Grammont and Irvine, 2001;Larkin et al, 1996;Xu et al, 1992). During late oogenesis, N signaling is required for the switch from the mitotic cycle to the endocycle and differentiation of follicle cells by negatively regulating the cut gene (Shcherbata et al, 2004;Sun and Deng, 2005), and it is also required for patterning the anterior egg shell (Dobens et al, 2005). In this study, we have shown, for the first time to our knowledge, that N signaling is necessary and sufficient for controlling formation of the GSC niche.…”

Section: Introductionmentioning

confidence: 56%

Notch signaling controls germline stem cell niche formation in theDrosophilaovary

et al. 2007

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Stem cells, which can self-renew and generate differentiated cells, have been shown to be controlled by surrounding microenvironments or niches in several adult tissues. However, it remains largely unknown what constitutes a functional niche and how niche formation is controlled. In the Drosophila ovary, germline stem cells (GSCs), which are adjacent to cap cells and two other cell types, have been shown to be maintained in the niche. In this study, we show that Notch signaling controls formation and maintenance of the GSC niche and that cap cells help determine the niche size in the Drosophila ovary. Expanded Notch activation causes the formation of more cap cells and bigger niches, which support more GSCs, whereas compromising Notch signaling during niche formation decreases the cap cell number and niche size and consequently the GSC number. Furthermore, the niches located away from their normal location can still sufficiently sustain GSC self-renewal by maintaining high local BMP signaling and repressing bam as in normal GSCs. Finally, loss of Notch function in adults results in rapid loss of the GSC niche, including cap cells and thus GSCs. Our results indicate that Notch signaling is important for formation and maintenance of the GSC niche, and that cap cells help determine niche size and function.

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Section: Introductionmentioning

confidence: 56%

Notch signaling controls germline stem cell niche formation in theDrosophilaovary

et al. 2007

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“…To determine whether miR-7 plays a role in regulating follicle cell differentiation, we overexpressed miR-7 (Stark et al, 2003) using the flip-out-GAL4 system (Pignoni and Zipursky, 1997). The normal cell-fate changes that occur in follicle cells can be revealed by staining for two transcription factors, Cut and Hindsight (Hnt), which have complementary expression patterns in follicle cells during oogenesis (Sun and Deng, 2005;Sun and Deng, 2007). Normally, Cut is expressed in early (stages 1-6) and late oogenesis (stage 10B to later), whereas Hnt is expressed only in midoogenesis (stages 7-10A), when follicle cells are undergoing endoreplication (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Immunocytochemistry and BrdU labeling were preformed as previously described (Sun and Deng, 2005) with the following antibodies: mouse antiBrdU (1:50; BD Bioscience), rabbit anti-Ttk69 (1:200; a gift from P. Badenhorst, University of Birmingham, UK), rabbit anti-VM32E (1:100; a gift from V. Cavaliere, University of Bologna, Italy), mouse anti-CD2 (1:50; AbD Serote), rabbit anti-β-Galactosidase (1:2000; MP Biomedicals), mouse anti-β-Galactosidase (1:500; Promega), mouse anti-Cut (2B10; 1:50) and mouse anti-Hnt (1G9; 1:15; Development Studies Hybridoma Bank). Nuclei were labeled with DAPI (Invitrogen).…”

Section: Immunocytochemistry Brdu Labeling and Imagingmentioning

confidence: 99%

The microRNA miR-7 regulates Tramtrack69 in a developmental switch in Drosophila follicle cells

et al. 2013

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SUMMARYDevelopment in multicellular organisms includes both small incremental changes and major switches of cell differentiation and proliferation status. During Drosophila oogenesis, the follicular epithelial cells undergo two major developmental switches that cause global changes in the cell-cycle program. One, the switch from the endoreplication cycle to a gene-amplification phase, during which special genomic regions undergo repeated site-specific replication, is attributed to Notch downregulation, ecdysone signaling activation and upregulation of the zinc-finger protein Tramtrack69 (Ttk69). Here, we report that the microRNA miR-7 exerts an additional layer of regulation in this developmental switch by regulating Ttk69 transcripts. miR-7 recognizes the 3′ UTR of ttk69 transcripts and regulates Ttk69 expression in a dose-dependent manner. Overexpression of miR-7 effectively blocks the switch from the endocycle to gene amplification through its regulation of ttk69. miR-7 and Ttk69 also coordinate other cell differentiation events, such as vitelline membrane protein expression, that lead to the formation of the mature egg. Our studies reveal the important role miR-7 plays in developmental decision-making in association with signal-transduction pathways.

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“…We also examined the expression of two Notch signaling targets, Cut and Hindsight (Hnt; Pebbled -FlyBase). In wild-type FCs, Cut expression is downregulated whereas Hnt expression is upregulated upon Notch activation at stage 6 (Sun and Deng, 2005;Sun and Deng, 2007). PI4KIIIalpha mutant PFCs frequently failed to downregulate Cut ( Fig.…”

Section: Research Reportmentioning

confidence: 92%

Drosophila PI4KIIIalpha is required in follicle cells for oocyte polarization and Hippo signaling

et al. 2011

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SUMMARYIn a genetic screen we isolated mutations in CG10260, which encodes a phosphatidylinositol 4-kinase (PI4KIIIalpha), and found that PI4KIIIalpha is required for Hippo signaling in Drosophila ovarian follicle cells. PI4KIIIalpha mutations in the posterior follicle cells lead to oocyte polarization defects similar to those caused by mutations in the Hippo signaling pathway. PI4KIIIalpha mutations also cause misexpression of well-established Hippo signaling targets. The Merlin-Expanded-Kibra complex is required at the apical membrane for Hippo activity. In PI4KIIIalpha mutant follicle cells, Merlin fails to localize to the apical domain. Our analysis of PI4KIIIalpha mutants provides a new link in Hippo signal transduction from the cell membrane to its core kinase cascade.

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Notch-dependent downregulation of the homeodomain gene cut is required for the mitotic cycle/endocycle switch and cell differentiation inDrosophilafollicle cells

Cited by 134 publications

References 57 publications

Notch signaling controls germline stem cell niche formation in theDrosophilaovary

Notch signaling controls germline stem cell niche formation in theDrosophilaovary

The microRNA miR-7 regulates Tramtrack69 in a developmental switch in Drosophila follicle cells

Drosophila PI4KIIIalpha is required in follicle cells for oocyte polarization and Hippo signaling

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