Misexpression screen delineates novel genes controlling Drosophila lifespanopen access
- Authors
- Paik, Donggi; Jang, Yeo Gil; Lee, Young Eun; Lee, Young Nam; Yamamoto, Rochelle; Gee, Heon Yung; Yoo, Seungmin; Bae, Eunkyung; Min, Kyung-Jin; Tatar, Marc; Park, Joong-Jean
- Issue Date
- May-2012
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- Aging; Misexpression screen; Longevity genes; ImpL2
- Citation
- MECHANISMS OF AGEING AND DEVELOPMENT, v.133, no.5, pp 234 - 245
- Pages
- 12
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- MECHANISMS OF AGEING AND DEVELOPMENT
- Volume
- 133
- Number
- 5
- Start Page
- 234
- End Page
- 245
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/12118
- DOI
- 10.1016/j.mad.2012.02.001
- ISSN
- 0047-6374
- Abstract
- In an initial preliminary screen we identified factors associated with controlling Drosophila aging by examining longevity in adults where EP elements induced over-expression or antisense-RNA at genes adjacent to each insertion. Here, we study 45 EP lines that initially showed at least 10% longer mean lifespan than controls. These 45 lines and a daughterless (da)-Gal4 stock were isogenized into a CS10 wild-type background. Sixteen EP lines corresponding to 15 genes significantly extended lifespan when their target genes were driven by da-Gal4. In each case, the target genes were seen to be over-expressed. Independently derived UAS-gene transgenic stocks were available or made for two candidates: ImpL2 which is ecdysone-inducible gene L2, and CG33138, 1,4-alpha-glucan branching enzyme. With both, adult lifespan was increased upon over-expression via the GeneSwitch inducible Gal4 driver system. Several genes in this set of 15 correspond to previously discovered longevity assurance systems such as insulin/IGF-1 signaling, gene silencing, and autophagy; others suggest new potential mechanisms for the control of aging including mRNA synthesis and maturation, intracellular vesicle trafficking, and neuroendocrine regulation. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
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Collections - 1. Basic Science > Department of Physiology > 1. Journal Articles
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