Abstract：
:Reactive oxygen species (ROS) are generated during physiological bouts of synaptic activity and as a consequence of pathological conditions in the central nervous system. How neurons respond to and distinguish between ROS in these different contexts is currently unknown. In Drosophila mutants with enhanced JNK activity, lower levels of ROS are observed and these animals are resistant to both changes in ROS and changes in synapse morphology induced by oxidative stress. In wild type flies, disrupting JNK-AP-1 signalling perturbs redox homeostasis suggesting JNK activity positively regulates neuronal antioxidant defense. We validated this hypothesis in mammalian neurons, finding that JNK activity regulates the expression of the antioxidant gene Srxn-1, in a c-Jun dependent manner. We describe a conserved 'adaptive' role for neuronal JNK in the maintenance of redox homeostasis that is relevant to several neurodegenerative diseases.
journal_name
Redox Bioljournal_title
Redox biologyauthors
Ugbode C,Garnham N,Fort-Aznar L,Evans GJO,Chawla S,Sweeney STdoi
10.1016/j.redox.2020.101712subject
Has Abstractpub_date
2020-10-01 00:00:00pages
101712issn
2213-2317pii
S2213-2317(20)30917-4journal_volume
37pub_type
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