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Induction and Detection of Oncogene-Induced Cellular Senescence in Drosophila

Part of the Methods in Molecular Biology book series (MIMB,volume 1534)

Abstract

Cellular senescence is induced by various cellular stresses, including activation of the Ras oncogene. In Drosophila imaginal epithelia, clones of cells expressing oncogenic Ras (RasV12) show several markers of cellular senescence, such as elevation of SA-β-gal activity, upregulation of the Cdk inhibitor Dacapo (Dap), and heterochromatinization. However, these cells do not undergo cell cycle arrest or exhibit a DNA damage response (DDR), cellular hypertrophy, or a senescence-associated secretory phenotype (SASP), other essential markers of cellular senescence. However, we found that inducing mitochondrial dysfunction within RasV12-expressing cells caused all above-mentioned aspects of cellular senescence. This provided the first evidence that cellular senescence occurs in invertebrates and is intriguing because mitochondrial dysfunction is frequently observed in human cancers. Here, we describe the procedures for the induction and detection of cellular senescence in Drosophila epithelia.

Key words

  • Cellular senescence
  • Drosophila
  • SASP
  • Ras
  • Mitochondrial dysfunction

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Acknowledgment

This work was supported in part by grants from the Ministry of Education, Culture, Sports, Science and Technology-Japan (MEXT) to T.I., the Japan Society for the Promotion of Science to M.N. and T.I., the Japan Science and Technology Agency to T.I., and the Takeda Science Foundation to T.I.

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Correspondence to Tatsushi Igaki Ph.D. .

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Nakamura, M., Igaki, T. (2017). Induction and Detection of Oncogene-Induced Cellular Senescence in Drosophila . In: Nikiforov, M. (eds) Oncogene-Induced Senescence. Methods in Molecular Biology, vol 1534. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-6670-7_20

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  • DOI: https://doi.org/10.1007/978-1-4939-6670-7_20

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  • Publisher Name: Humana Press, New York, NY

  • Print ISBN: 978-1-4939-6668-4

  • Online ISBN: 978-1-4939-6670-7

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