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Research Paper|Volume 6, Issue 12|pp 1076—1093

Embryonic expression of shuttle craft, a Drosophila gene involved in neuron development, is associated with adult lifespan

Natalia V. Roshina1, Alexander V. Symonenko1, Anna V. Krementsova1,2, Mikhail V. Trostnikov1, Elena G. Pasyukova1
  • 1Institute of Molecular Genetics of Russian Academy of Sciences, Moscow, 123182, Russia
  • 2Emmanuel Institute of Biochemical Physics of Russian Academy of Sciences, Moscow, 119334, Russia

* * Equal contribution

Received: October 28, 2014Accepted: December 27, 2014Published: December 28, 2014

Copyright: © 2014 Roshina et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Despite the progress in aging research that highlights the role of the nervous system in longevity, whether genes that control development and consequently structure of the nervous system affect lifespan is unclear. We demonstrated that a mutation in shuttle craft, a gene involved in the nervous system development, increased the lifespan of unmated females and decreased the lifespan of mated females, without affecting males. Precise reversions of the mutation lead to the restoration of the lifespan specific to control females. In mutant unmated females, increased lifespan was associated with elevated locomotion at older ages, indicating slowed aging. In mutant mated females, reproduction was decreased compared to controls, indicating a lack of tradeoff between this trait and lifespan. No differences in shuttle craft transcription were observed between whole bodies, ovaries, and brains of mutant and control females of different ages, either unmated or mated. The amount of shuttle craft transcript appeared to be substantially decreased in mutant embryos. Our results demonstrated that a gene that regulates development of the nervous system might also influence longevity, and thus expanded the spectrum of genes involved in lifespan control. We hypothesize that this “carry-over” effect might be the result of transcription regulation in embryos.