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The Neuropeptide PDF Is Crucial for Delaying the Phase of Drosophila's Evening Neurons Under Long Zeitgeber Periods.

ABSTRACT: Circadian clocks schedule biological functions at a specific time of the day. Full comprehension of the clock function requires precise understanding of their entrainment to the environment. The phase of entrained clock is plastic, which depends on different factors such as the period of endogenous oscillator, the period of the zeitgeber cycle (T), and the proportion of light and darkness (day length). The circadian clock of fruit fly Drosophila melanogaster is able to entrain to a wide range of T-cycles and day lengths. Here, we investigated the importance of the neuropeptide Pigment-Dispersing Factor (PDF) for entrainment by systematically studying locomotor activity rhythms of Pdf ⁰ mutants and wild-type flies under different T-cycles (T22 to T32) and different day lengths (8, 12, and 16 hour [h]). Furthermore, we analysed PERIOD protein oscillations in selected groups of clock neurons in both genotypes under T24 and T32 at a day length of 16 h. As expected, we found that the phase of Drosophila's evening activity and evening neurons advanced with increasing T in all the day lengths. This advance was much larger in Pdf ⁰ mutants (~7 h) than in wild-type flies causing (1) pronounced desynchrony between morning and evening neurons and (2) evening activity to move in the morning instead of the evening. Most interestingly, we found that the lights-off transition determines the phase of evening neurons in both genotypes and that PDF appears necessary to delay the evening neurons by ~3 h to their wild-type phase. Thus, in T32, PDF first delays the molecular cycling in the evening neurons, and then, as shown in previous studies, delays their neuronal firing rhythms to produce a total delay of ~7 h necessary for a wild-type evening activity phase. We conclude that PDF is crucial for appropriate phasing of Drosophila activity rhythm.

SUBMITTER: Vaze KM

PROVIDER: S-EPMC8442139 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Background The risk of cardiovascular disease is known to increase after menopause. Mitochondria, which undergo quality control via mitochondrial autophagy, play a crucial role in the regulation of cellular senescence. The aim of this study was to investigate whether the effect of estrogen-mediated protection from senescence on arteries is attributed to the induction of mitochondrial autophagy. Methods and Results We used human umbilical vein cells, vascular smooth muscle cells, and 12-week-old female C57BL/6 mice. The administration of 17β-estradiol (E2) to cells inhibited cellular senescence and mitochondrial dysfunction. Furthermore, E2 increased mitochondrial autophagy, maintaining mitochondrial function, and retarding cellular senescence. Of note, E2 did not modulate LC3 (light chain 3), and ATG7 (autophagy related 7) deficiency did not suppress mitochondrial autophagy in E2-treated cells. Conversely, E2 increased the colocalization of Rab9 with LAMP2 (lysosomal-associated membrane protein 2) signals. The E2-mediated effects on mitochondrial autophagy were abolished by the knockdown of either Ulk1 or Rab9. These results suggest that E2-mediated mitochondrial autophagy is associated with Rab9-dependent alternative autophagy. E2 upregulated SIRT1 (sirtuin 1) and activated LKB1 (liver kinase B1), AMPK (adenosine monophosphate-activated protein kinase), and Ulk1, indicating that the effect of E2 on the induction of Rab9-dependent alternative autophagy is mediated by the SIRT1/LKB1/AMPK/Ulk1 pathway. Compared with the sham-operated mice, ovariectomized mice showed reduced mitochondrial autophagy and accelerated mitochondrial dysfunction and arterial senescence; these detrimental alterations were successfully rescued by the administration of E2. Conclusions We showed that E2-induced mitochondrial autophagy plays a crucial role in the delay of vascular senescence. The Rab9-dependent alternative autophagy is behind E2-induced mitochondrial autophagy.

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The Neuropeptide PDF Is Crucial for Delaying the Phase of Drosophila's Evening Neurons Under Long Zeitgeber Periods.

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