Biology subjects

Poe, A. R.

Publications and source records attributed to Poe, A. R..

6 recordsLinked to original sources

bioRxiv2026

Development of Circadian Circuitry Underlying Feeding-Fasting Rhythms in Drosophila Larvae

Many organisms do not exhibit strong daily behavioral rhythms early in life. The consolidation of sleep and feeding to specific times of the day does not emerge until later in development. Disruptions to circadian behaviors in early life can lead to dysregulation of both neural development and metabolic homeostasis. However, the circuit mechanisms regulating feeding rhythm development are unknown. Here, we characterize the neural circuitry responsible for driving the development of feeding-fasting rhythms in early 3rd instar (L3) Drosophila larvae. We find that inactivation of both larval s-LNv circadian pacemaker neurons and SIFamide (SIFa) neurons in the pars intercerebralis disrupts feeding rhythm development. Additionally, our data indicate feeding rhythms likely emerge due to circuit connections forming between s-LNvs and SIFa neurons at the L3 stage. Finally, we show that reductions in signaling between s-LNv and SIFa neurons interfere with normal behavioral rhythm development in L3. Specifically, RNA interference-induced reductions in pigment-dispersing factor (pdf) signaling and SIFa signaling disrupt diurnal differences in both feeding and sleep, resulting in a loss of behavioral rhythms. Altogether, our findings identify for the first time the clock and clock output circuitry responsible for feeding rhythm regulation in developing organisms.

neuroscience↗

bioRxiv2026

Nutritional Regulation of DN1a-Dh44 Signaling Modulates Sleep Across the Lifespan

Across species, sleep amount and timing are tightly linked to the nutritional environment. While early life sleep and sleep in mature organisms are both dramatically influenced by reductions in the dietary environment, the mechanisms linking nutritional cues to conserved sleep-regulatory circuitry are not well understood. Using both early 3rd instar (L3) Drosophila larvae and adults, we examined the plasticity of sleep responses under shifting nutrient environments across the lifespan. We find that L3 larvae and adults exhibit changes in sleep duration in low sugar environments with L3 showing a loss of sleep-wake rhythms that can be rescued with additional nutrients. We show that larval and adult sleep plasticity is regulated by CCHamide-1 signaling between DN1a and Dh44 neurons and glucose metabolic genes in Dh44 neurons. Additionally, our data indicate that sleep plasticity is not dependent on anatomical and functional connectivity between clock-arousal circuitry, suggesting that peptidergic signaling alone is sufficient for diet-dependent sleep regulation. Finally, we demonstrate that Dh44 neurons in both L3 larvae and adults adjust mRNA levels of CCHamide-1 receptor (CCHa1-R) in response to changes in dietary sugar. Together, our findings suggest that organisms utilize conserved molecular signaling pathways across the lifespan to dynamically regulate their sleep in a changing environment.

neuroscience↗

bioRxiv2023

Energetic Demands Regulate Sleep-Wake Rhythm Circuit Development

Sleep and feeding patterns lack strong daily rhythms during early life. As diurnal animals mature, feeding is consolidated to the day and sleep to the night. In Drosophila, circadian sleep patterns are initiated with formation of a circuit connecting the central clock to arousal output neurons; emergence of circadian sleep also enables long-term memory (LTM). However, the cues that trigger the development of this clock-arousal circuit are unknown. Here, we identify a role for nutritional status in driving sleep-wake rhythm development in Drosophila larvae. We find that in the 2nd instar larval period (L2), sleep and feeding are spread across the day; these behaviors become organized into daily patterns by the 3rd instar larval stage (L3). Forcing mature (L3) animals to adopt immature (L2) feeding strategies disrupts sleep-wake rhythms and the ability to exhibit LTM. In addition, the development of the clock (DN1a)-arousal (Dh44) circuit itself is influenced by the larval nutritional environment. Finally, we demonstrate that larval arousal Dh44 neurons act through glucose metabolic genes to drive onset of daily sleep-wake rhythms. Together, our data suggest that changes to energetic demands in developing organisms trigger the formation of sleep-circadian circuits and behaviors.

neuroscience↗

bioRxiv2022

Developmental emergence of sleep rhythms enables long-term memory capabilities in Drosophila

In adulthood, sleep-wake rhythms are one of the most prominent behaviors under circadian control. However, during early life, sleep is spread across the 24-hour day (1-4). The mechanism through which sleep rhythms emerge, and the consequent advantage conferred to a juvenile animal, are unknown. In 2nd instar Drosophila larvae (L2), like human infants, sleep is not under circadian control (5). Here, we identify the precise developmental timepoint when the circadian clock begins to regulate sleep in Drosophila, leading to the emergence of sleep rhythms at the early 3rd instar stage (L3). At this stage, a cellular connection forms between DN1a clock neurons and arousalpromoting Dh44 neurons, bringing arousal under clock control to drive the emergence of circadian sleep. Finally, we demonstrate that L3 but not L2 larvae exhibit long-term memory (LTM) of an aversive cue, and that this LTM depends upon deep sleep generated once sleep rhythms begin. We propose that the developmental emergence of circadian sleep enables more complex cognitive processes, including the onset of enduring memories.

neuroscience↗

bioRxiv2019

Low FoxO expression in Drosophila somatosensory neurons protects dendrite growth under nutrient restriction

During prolonged nutrient restriction, developing animals redistribute vital nutrients to favor brain growth at the expense of other organs. In Drosophila, such brain sparing relies on a glia-derived growth factor to sustain proliferation of neural stem cells. However, whether other aspects of neural development are also spared under nutrient restriction is unknown. Here we show that dynamically growing somatosensory neurons in the Drosophila peripheral nervous system exhibit organ sparing at the level of arbor growth: Under nutrient stress, sensory dendrites preferentially grow as compared to neighboring non-neural tissues, resulting in dendrite overgrowth. Underlying this neuronal nutrient-insensitivity is the lower expression of the stress sensor FoxO in neurons. Consequently, nutrient restriction suppresses Tor signaling less and does not induce autophagy in neurons. Preferential dendrite growth is functional desirable because it results in heightened animal responses to sensory stimuli, indicative of a potential survival advantage under environmental challenges.

neuroscience↗

bioRxiv2018

Highly efficient CRISPR/Cas9-mediated tissue specific mutagenesis in Drosophila

Tissue-specific loss-of-function (LOF) analysis is an essential approach for characterizing gene function. Here we describe an efficient CRISPR-mediated tissue-restricted mutagenesis (CRISPR-TRiM) method for ablating gene function in Drosophila. This binary system consists of a tissue-specific Cas9 and a ubiquitously expressed multi-guide RNA (gRNA) transgene. To facilitate the construction of these components, we developed convenient tools for generating and evaluating enhancer-driven Cas9 lines, identified a multi-gRNA design that is highly efficient in mutagenizing somatic cells, and established an assay for testing the efficiency of multi-gRNAs in creating double-stranded breaks. We found that excision of genomic DNA induced by two gRNAs is infrequent in somatic cells, while indels more reliably cause tissue-specific LOF. Furthermore, we show that enhancer-driven Cas9 is less cytotoxic yet results in more complete gene removal than Gal4-driven Cas9 in larval neurons. Finally, we demonstrate that CRISPR-TRiM efficiently unmasks redundant gene functions in neuronal morphogenesis. Importantly, two Cas9 transgenes that turn on with different timings in the neuronal lineage revealed the extent to which gene products persist in cells after tissue-specific gene knockout. These CRISRPR tools can be applied to analyze tissue-specific gene function in many biological processes.

developmental biology↗