TY  - GEN
T1  - Differential effects on neuromuscular physiology between Sod1 loss-of-function mutation and paraquat-induced oxidative stress in Drosophila
AU  - Ueda, Atsushi
AU  - Iyengar, Atulya
AU  - Wu, Chun-Fang
DO  - 10.17912/micropub.biology.000385
UR  - http://beta.micropublication.org/journals/biology/micropub-biology-000385/
AB  - Free radicals, such as the superoxide anion (O2–) impart oxidative stress upon an animal and are thought to be a major contributing factor to age-related changes in the nervous system (Finkel & Holbrook, 2000; Harman, 1956; Harman, 1981). In eukaryotes, the cytosolic enzyme Cu2+/Zn2+ Superoxide Dismutase (in Drosophila encoded by Sod1, originally cSOD, Campbell et al., 1986) is an important free radical scavenger that converts superoxide into hydrogen peroxide. Drosophila Sod1 loss-of-function mutants exhibit elevated levels of reactive oxygen species (ROS) combined with a drastically shortened adult lifespan (median ~11 d. vs 50 d. for wild-type flies at 25 °C, Phillips et al., 1989) and reduced locomotor ability in larvae (Şahin et al., 2017) and adults (Ruan & Wu, 2008). Coupled with these longevity and behavioral phenotypes, several neuromuscular deficits have recently been identified in Sod1 loss-of-function mutants including deranged nerve and synapse morphology in larvae (Milton et al., 2011) and adults (Agudelo et al., 2020; Şahin et al., 2017), as well as disrupted neurotransmission along the giant-fiber (GF) jump-and-flight escape circuit (Iyengar et al., 2020; Iyengar, 2016; Ruan, 2008). Given the striking phenotypes, a question that arises is: To what extent the straightforward assumption holds that aspects of the Sod1 phenotypes can be recapitulated by pharmacologically induced oxidative stress?
PY  - 2021
JO  - microPublication Biology
ER  -