Myc in model organisms: A view from the flyroom

Cova, Claire de la; Johnston, Laura

doi:10.1016/j.semcancer.2006.07.010

Cited by 37 publications

(39 citation statements)

References 53 publications

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“…This type of 'classical' cell competition has also been documented in the case of Myc, a transcription factor that regulates expression of genes controlling proliferation, cellular growth and ribosome biogenesis (de la Cova et al, 2004;Moreno and Basler, 2004;de la Cova and Johnston, 2006). Animals with hypomorphic mutations in Myc [encoded by the diminutive (dm) gene] are viable but grow more slowly and are smaller than wild-type flies.…”

Section: Introductionmentioning

confidence: 93%

Activated STAT regulates growth and induces competitive interactions independently of Myc, Yorkie, Wingless and ribosome biogenesis

et al. 2012

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SUMMARYCell competition is a conserved mechanism that regulates organ size and shares properties with the early stages of cancer. In Drosophila, wing cells with increased Myc or with optimum ribosome function become supercompetitors that kill their wild-type neighbors (called losers) up to several cell diameters away. Here, we report that modulating STAT activity levels regulates competitor status. Cells lacking STAT become losers that are killed by neighboring wild-type cells. By contrast, cells with hyper-activated STAT become supercompetitors that kill losers located at a distance in a manner that is dependent on hid but independent of Myc, Yorkie, Wingless signaling, and of ribosome biogenesis. These results indicate that STAT, Wingless and Myc are major parallel regulators of cell competition, which may converge on signals that non-autonomously kill losers. As hyper-activated STATs are causal to tumorigenesis and stem cell niche occupancy, our results have therapeutic implications for cancer and regenerative medicine.

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Section: Introductionmentioning

confidence: 93%

Activated STAT regulates growth and induces competitive interactions independently of Myc, Yorkie, Wingless and ribosome biogenesis

et al. 2012

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“…By phosphorylating and sequestering Foxo in the cytoplasm, Akt further promotes cell growth and cell cycle progression (Accili and Arden, 2004;Greer and Brunet, 2008;Puig and Tjian, 2006). Similar to InR/Tor signaling, Myc has an evolutionarily conserved function in promoting cell growth and proliferation (de la Cova and Johnston, 2006). Myc regulates gene expression by binding to Enhancer box sequences (E-boxes) in promoter regions of target genes, with its dimerization partner Max, but also independently (Steiger et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Integration of Insulin receptor/Foxo signaling and dMyc activity during muscle growth regulates body size inDrosophila

2009

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Drosophila larval skeletal muscles are single, multinucleated cells of different sizes that undergo tremendous growth within a few days. The mechanisms underlying this growth in concert with overall body growth are unknown. We find that the size of individual muscles correlates with the number of nuclei per muscle cell and with increasing nuclear ploidy during development. Inhibition of Insulin receptor (InR; Insulin-like receptor) signaling in muscles autonomously reduces muscle size and systemically affects the size of other tissues, organs and indeed the entire body, most likely by regulating feeding behavior. In muscles, InR/Tor signaling, Foxo and dMyc (Diminutive) are key regulators of endoreplication, which is necessary but not sufficient to induce growth. Mechanistically, InR/Foxo signaling controls cell cycle progression by modulating dmyc expression and dMyc transcriptional activity. Thus, maximal dMyc transcriptional activity depends on InR to control muscle mass, which in turn induces a systemic behavioral response to allocate body size and proportions.

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“…During normal development and tissue homeostasis, Myc controls several cellular processes, most prominently growth, proliferation and apoptosis (de la Cova and Johnston, 2006;Pirity et al, 2006). These different activities of Myc have been attributed to its ability to stimulate or repress the transcription of many target genes (reviewed by Grandori et al, 2000;Amati et al, 2001;Dang et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

The conserved Myc box 2 and Myc box 3 regions are important, but not essential, for Myc function in vivo

Schwinkendorf¹,

Gallant²

2009

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Myc in model organisms: A view from the flyroom

Cited by 37 publications

References 53 publications

Activated STAT regulates growth and induces competitive interactions independently of Myc, Yorkie, Wingless and ribosome biogenesis

Activated STAT regulates growth and induces competitive interactions independently of Myc, Yorkie, Wingless and ribosome biogenesis

Integration of Insulin receptor/Foxo signaling and dMyc activity during muscle growth regulates body size inDrosophila

The conserved Myc box 2 and Myc box 3 regions are important, but not essential, for Myc function in vivo

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