When cell cycle meets development

Kaldis, Philipp; Richardson, Helena E.

doi:10.1242/dev.073288

Cited by 21 publications

(20 citation statements)

References 34 publications

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“…However, how developmental cues controlling the cell cycle in different developmental situations remains to be addressed 15 . Because miR-17-92 and E2F family play pivotal roles in the cell cycle control, we hypothesized that the auto-regulatory feedback loop between mir-17-92 and E2F family may regulate palate development via cell cycle modulation.…”

Section: Resultsmentioning

confidence: 99%

An E2F1/MiR-17-92 Negative Feedback Loop mediates proliferation of Mouse Palatal Mesenchymal Cells

Shi

Chen

et al. 2017

Sci Rep

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Normal cell cycle progression and proliferation of palatal mesenchymal cells are important for palatal development. As targets of miR-17-92, E2F transcription factors family has been suggested to induce the transcription of miR-17-92 in several cell types. In the present study, we sought to investigate whether this negative feedback loop exists in mouse PMCs and what the function of this negative feedback loop would be in palatal mesenchymal cells. Using GeneMANIA, we revealed that the most important function of experimentally verified targets of miR-17-92 is cell cycle regulation. E2F1 and E2F3, but not E2F2, were extensively expressed in mouse palate. Over-expression of E2F1 significantly increased the expression of all the members of miR-17-92. After increased by E2F1, miR-17 and miR-20a may negatively target E2F1, and thereby prevent the cells from excessive proliferation. We suggest that the negative feedback loop between E2F1 and miR-17-92 may contribute to palatal development by regulating the proliferation and cell cycle of palatal mesenchymal cells.

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Section: Resultsmentioning

confidence: 99%

An E2F1/MiR-17-92 Negative Feedback Loop mediates proliferation of Mouse Palatal Mesenchymal Cells

Shi

Chen

et al. 2017

Sci Rep

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“…RA), and cell cycle genes involved have been described in a few systems, including neuronal progenitor cells (Chen et al, 2012;Diez del Corral et al, 2003;Seo et al, 2005a). Little is known about the molecular nature of the switch that controls the shift between proliferation of neural precursors and their entry into the neuronal differentiation pathway (Kaldis and Richardson, 2012).…”

Section: Discussion Rar Signaling Promotes Neuronal Differentiationmentioning

confidence: 99%

ERF and ETV3L are retinoic acid-inducible repressors required for primary neurogenesis

et al. 2013

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SUMMARYCells in the developing neural tissue demonstrate an exquisite balance between proliferation and differentiation. Retinoic acid (RA) is required for neuronal differentiation by promoting expression of proneural and neurogenic genes. We show that RA acts early in the neurogenic pathway by inhibiting expression of neural progenitor markers Geminin and Foxd4l1, thereby promoting differentiation. Our screen for RA target genes in early Xenopus development identified Ets2 Repressor Factor (Erf) and the closely related ETS repressors Etv3 and Etv3-like (Etv3l). Erf and Etv3l are RA responsive and inhibit the action of ETS genes downstream of FGF signaling, placing them at the intersection of RA and growth factor signaling. We hypothesized that RA regulates primary neurogenesis by inducing Erf and Etv3l to antagonize proliferative signals. Loss-of-function analysis showed that Erf and Etv3l are required to inhibit proliferation of neural progenitors to allow differentiation, whereas overexpression of Erf led to an increase in the number of primary neurons. Therefore, these RA-induced ETS repressors are key components of the proliferation-differentiation switch during primary neurogenesis in vivo.

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“…Thus, KSHV, like EBV, reactivates by exploiting the terminal differentiation pathway of latently infected B cells. In most cell lineages, final differentiation is associated with loss of proliferation and cell cycle arrest in G 1 phase (52). During the differentiation process, the expression of various CDKIs, including p27, is upregulated.…”

Section: Discussionmentioning

confidence: 99%

Kaposi's Sarcoma-Associated Herpesvirus Transactivator Rta Induces Cell Cycle Arrest in G ₀ /G ₁ Phase by Stabilizing and Promoting Nuclear Localization of p27 ^kip

Kumar

Wood

2013

J Virol

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The Kaposi's sarcoma-associated herpesvirus (KSHV) immediate-early gene, replication, and transcription activator (K-Rta) is a key viral protein that serves as the master regulator for viral lytic replication. In this study, we investigated the role of K-Rta in cell cycle regulation and found that the expression of K-Rta in doxycycline (Dox)-inducible BJAB cells induced cell cycle arrest in G 0 /G 1 phase. Western blot analysis of key cell cycle regulators revealed that K-Rta-mediated cell cycle arrest was associated with a decrease in cyclin A and phosphorylated Rb (pS807/pS811) protein levels, both markers of S phase progression, and an increase in protein levels for p27, a cyclin-dependent kinase inhibitor. Further, we found that K-Rta does not affect the transcription of p27 but regulates p27 at the posttranslational level by inhibiting its proteosomal degradation. Immunofluorescence staining and cell fractionation experiments revealed largely nuclear compartmentalization of p27 in K-Rta-expressing cells, demonstrating that K-Rta not only stabilizes p27 but also modulates its cellular localization. Finally, short hairpin RNA knockdown of p27 significantly abrogates cell cycle arrest in K-Rta-expressing cells, supporting its key role in K-Rta-mediated cell cycle arrest. Our findings are consistent with previous studies which showed that expression of immediate-early genes of several herpesviruses, including herpes simplex virus, Epstein-Barr virus, and cytomegalovirus, results in cell cycle arrest at the G 0 /G 1 phase, possibly to avoid competition for resources needed for host cell replication during the S phase.

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When cell cycle meets development

Cited by 21 publications

References 34 publications

An E2F1/MiR-17-92 Negative Feedback Loop mediates proliferation of Mouse Palatal Mesenchymal Cells

An E2F1/MiR-17-92 Negative Feedback Loop mediates proliferation of Mouse Palatal Mesenchymal Cells

ERF and ETV3L are retinoic acid-inducible repressors required for primary neurogenesis

Kaposi's Sarcoma-Associated Herpesvirus Transactivator Rta Induces Cell Cycle Arrest in G ₀ /G ₁ Phase by Stabilizing and Promoting Nuclear Localization of p27 ^kip

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When cell cycle meets development

Cited by 21 publications

References 34 publications

An E2F1/MiR-17-92 Negative Feedback Loop mediates proliferation of Mouse Palatal Mesenchymal Cells

An E2F1/MiR-17-92 Negative Feedback Loop mediates proliferation of Mouse Palatal Mesenchymal Cells

ERF and ETV3L are retinoic acid-inducible repressors required for primary neurogenesis

Kaposi's Sarcoma-Associated Herpesvirus Transactivator Rta Induces Cell Cycle Arrest in G 0 /G 1 Phase by Stabilizing and Promoting Nuclear Localization of p27 kip

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Kaposi's Sarcoma-Associated Herpesvirus Transactivator Rta Induces Cell Cycle Arrest in G ₀ /G ₁ Phase by Stabilizing and Promoting Nuclear Localization of p27 ^kip