Drosophila Clock Is Required in Brain Pacemaker Neurons to Prevent Premature Locomotor Aging Independently of Its Circadian Function
Identifieur interne : 001B97 ( Ncbi/Curation ); précédent : 001B96; suivant : 001B98Drosophila Clock Is Required in Brain Pacemaker Neurons to Prevent Premature Locomotor Aging Independently of Its Circadian Function
Auteurs : Alexandra Vaccaro [France] ; Abdul-Raouf Issa [France] ; Laurent Seugnet [France] ; Serge Birman [France] ; André Klarsfeld [France]Source :
- PLoS Genetics [ 1553-7390 ] ; 2017.
Abstract
Circadian clocks control many self-sustained rhythms in physiology and behavior with approximately 24-hour periodicity. In many organisms, oxidative stress and aging negatively impact the circadian system and sleep. Conversely, loss of the clock decreases resistance to oxidative stress, and may reduce lifespan and speed up brain aging and neurodegeneration. Here we examined the effects of clock disruptions on locomotor aging and longevity in
Url:
DOI: 10.1371/journal.pgen.1006507
PubMed: 28072817
PubMed Central: 5224980
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PMC:5224980Le document en format XML
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Clock Is Required in Brain Pacemaker Neurons to Prevent Premature Locomotor Aging Independently of Its Circadian Function</title>
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Clock Is Required in Brain Pacemaker Neurons to Prevent Premature Locomotor Aging Independently of Its Circadian Function</title>
<author><name sortKey="Vaccaro, Alexandra" sort="Vaccaro, Alexandra" uniqKey="Vaccaro A" first="Alexandra" last="Vaccaro">Alexandra Vaccaro</name>
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<series><title level="j">PLoS Genetics</title>
<idno type="ISSN">1553-7390</idno>
<idno type="eISSN">1553-7404</idno>
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<front><div type="abstract" xml:lang="en"><p>Circadian clocks control many self-sustained rhythms in physiology and behavior with approximately 24-hour periodicity. In many organisms, oxidative stress and aging negatively impact the circadian system and sleep. Conversely, loss of the clock decreases resistance to oxidative stress, and may reduce lifespan and speed up brain aging and neurodegeneration. Here we examined the effects of clock disruptions on locomotor aging and longevity in <italic>Drosophila</italic>
. We found that lifespan was similarly reduced in three arrhythmic mutants (<italic>Clk</italic>
<sup>AR</sup>
, <italic>cyc</italic>
<sup>0</sup>
and <italic>tim</italic>
<sup>0</sup>
) and in wild-type flies under constant light, which stops the clock. In contrast, <italic>Clk</italic>
<sup>AR</sup>
mutants showed significantly faster age-related locomotor deficits (as monitored by startle-induced climbing) than <italic>cyc</italic>
<sup>0</sup>
and <italic>tim</italic>
<sup>0</sup>
, or than control flies under constant light. Reactive oxygen species accumulated more with age in <italic>Clk</italic>
<sup>AR</sup>
mutant brains, but this did not appear to contribute to the accelerated locomotor decline of the mutant. Clk, but not Cyc, inactivation by RNA interference in the pigment-dispersing factor (PDF)-expressing central pacemaker neurons led to similar loss of climbing performance as <italic>Clk</italic>
<sup>AR</sup>
. Conversely, restoring Clk function in these cells was sufficient to rescue the <italic>Clk</italic>
<sup>AR</sup>
locomotor phenotype, independently of behavioral rhythmicity. Accelerated locomotor decline of the <italic>Clk</italic>
<sup>AR</sup>
mutant required expression of the PDF receptor and correlated to an apparent loss of dopaminergic neurons in the posterior protocerebral lateral 1 (PPL1) clusters. This neuronal loss was rescued when the <italic>Clk</italic>
<sup>AR</sup>
mutation was placed in an apoptosis-deficient background. Impairing dopamine synthesis in a single pair of PPL1 neurons that innervate the mushroom bodies accelerated locomotor decline in otherwise wild-type flies. Our results therefore reveal a novel circadian-independent requirement for Clk in brain circadian neurons to maintain a subset of dopaminergic cells and avoid premature locomotor aging in <italic>Drosophila</italic>
.</p>
</div>
</front>
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