Questions, Feedback & Help
Send us an email and we'll get back to you ASAP. Or you can read our Frequently Asked Questions.
  • page settings
  • hide sidebar
  • show empty fields
  • layout
  • (too narrow)
  • open all
  • close all
Resources » Paper

Schlotterer, Andreas et al. (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "Apurinic/apyrimidinic endonuclease 1 and mitochondrial ROS are linked to age-related declines in neuronal structure and function in C. elegans"

  • History

  • Referenced

  • Tree Display

  • My Favorites

  • My Library

  • Comments on Schlotterer, Andreas et al. (2010) C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany "Apurinic/apyrimidinic endonuclease 1 and mitochondrial ROS are linked to age-related declines in neuronal structure and function in C. elegans" (0)

  • Overview

    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00036975

    Schlotterer, Andreas, Kukudov, Georgi, Bierhaus, Angelika, Nawroth, Peter, & Morcos, Michael (2010). Apurinic/apyrimidinic endonuclease 1 and mitochondrial ROS are linked to age-related declines in neuronal structure and function in C. elegans presented in C. elegans: Development and Gene Expression, EMBL, Heidelberg, Germany. Unpublished information; cite only with author permission.

    Major age-related changes include biochemical and morphological alterations, as well as a decline in neuromuscular function. To identify factors that control aging by modulating changes on all three levels, we have established C. elegans as a model organism for analysing the impact of aging, genetic control and pharmacological intervention on the formation of mitochondrial DNA (mtDNA) deletions, changes in neuronal morphology, and the progressive degeneration of neuronal functions involved in body movement. During aging of C. elegans , expression of the apurinic/apyrimidinic endonuclease 1 (APE1) ortholog exo-3 , a central component in the mitochondrial repair system of oxidative DNA damage, is reduced by 45% ( P <0.05). In parallel, an increased generation of reactive oxygen species (ROS) was observed and particularly colocalized with the nervous system. Although no structural damage of the nervous system could be detected up to the age of 12 days, functional parameters of neuromuscular behaviour were affected: head motility decreased from 0.174 to 0.095 mm s -1 ( P <0.001) and whole animal motility decreased from 0.108 to 0.041 mm s -1 ( P <0.001). Consistently, suppression of exo-3 by RNAi resulted in a 3-fold increase of mtDNA deletions ( P <0.05), 2-fold enhanced generation of ROS ( P <0.01), neuronal structural deterioration, reduction of head motility by 43% ( P <0.01) and whole animal motility by 38% ( P <0.05), and decrease of the mean lifespan from 18.50.4 to 15.40.1 days ( P <0.001) and the maximum lifespan from 25.90.4 to 23.20.1 days ( P =0 .001). In animals with downregulated exo-3 , reduction of mtROS decreased overall ROS levels, reduced neuronal damage, and increased motility and lifespan. These results demonstrate for the first time that levels of APE1/EXO-3 expression and mtROS formation are closely linked to age-related declines in neuronal structure and function in C. elegans .


    Tip: Seeing your name marked red? Please help us identify you.