Effects of MUL1 and PARKIN on the circadian clock, brain and behaviour in Drosophila Parkinson's disease models.
Animals
Animals, Genetically Modified
/ physiology
Brain
/ metabolism
CLOCK Proteins
/ biosynthesis
Circadian Clocks
/ physiology
Circadian Rhythm
/ physiology
Disease Models, Animal
Drosophila
Drosophila Proteins
/ biosynthesis
Locomotion
/ physiology
Longevity
/ physiology
Motor Skills
/ physiology
Mutation
Neurons
/ metabolism
Parkinson Disease
/ metabolism
Reactive Oxygen Species
/ metabolism
Sleep
/ physiology
Superoxide Dismutase
/ metabolism
Ubiquitin-Protein Ligases
/ genetics
Autophagy
Clock genes
Clock neurons
Locomotor activity rhythm
Mitochondrial ligases
ROS
SOD1
Sleep
Journal
BMC neuroscience
ISSN: 1471-2202
Titre abrégé: BMC Neurosci
Pays: England
ID NLM: 100966986
Informations de publication
Date de publication:
28 05 2019
28 05 2019
Historique:
received:
04
03
2019
accepted:
15
05
2019
entrez:
30
5
2019
pubmed:
30
5
2019
medline:
29
1
2020
Statut:
epublish
Résumé
Mutants which carry mutations in genes encoding mitochondrial ligases MUL1 and PARKIN are convenient Drosophila models of Parkinson's disease (PD). In several studies it has been shown that in Parkinson's disease sleep disturbance occurs, which may be the result of a disturbed circadian clock. We found that the ROS level was higher, while the anti-oxidant enzyme SOD1 level was lower in mul1 All of the changes observed in the brains of these Drosophila models of PD, in which mitochondrial ligases MUL1 and PARKIN do not function, may explain the mechanisms of some neurological and behavioural symptoms of PD.
Sections du résumé
BACKGROUND
Mutants which carry mutations in genes encoding mitochondrial ligases MUL1 and PARKIN are convenient Drosophila models of Parkinson's disease (PD). In several studies it has been shown that in Parkinson's disease sleep disturbance occurs, which may be the result of a disturbed circadian clock.
RESULTS
We found that the ROS level was higher, while the anti-oxidant enzyme SOD1 level was lower in mul1
CONCLUSIONS
All of the changes observed in the brains of these Drosophila models of PD, in which mitochondrial ligases MUL1 and PARKIN do not function, may explain the mechanisms of some neurological and behavioural symptoms of PD.
Identifiants
pubmed: 31138137
doi: 10.1186/s12868-019-0506-8
pii: 10.1186/s12868-019-0506-8
pmc: PMC6540415
doi:
Substances chimiques
Atg5 protein, Drosophila
0
Drosophila Proteins
0
Reactive Oxygen Species
0
Sod1 protein, Drosophila
EC 1.15.1.1
Superoxide Dismutase
EC 1.15.1.1
CLOCK Proteins
EC 2.3.1.48
Ubiquitin-Protein Ligases
EC 2.3.2.27
mitochondrial ubiquitin ligase 1, Drosophila
EC 2.3.2.27
parkin protein
EC 2.3.2.27
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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