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De, J.

Publications and source records attributed to De, J..

3 recordsLinked to original sources

Genetic sex of enteric neurons enables ovarian relaxin togate maternal gut plasticity

Animals must align intestinal plasticity and feeding with reproductive state, yet the checkpoint that gates these adaptations is unknown. Here we show that an ovary-to-enteric-neuron axis gates the onset of maternal gut plasticity in Drosophila. Genetic sex establishes endocrine competence in a subset of enteric neurons via the sex determination pathway, enabling female-specific expression of the relaxin-family receptor Lgr3. After mating, steroid signalling increases Lgr3 receptor expression, priming these neurons for reproductive adaptation. Once oocytes mature fully, follicle cells secrete the relaxin-like hormone dILP8, which activates Lgr3 to trigger gut enlargement and increased feeding. Disrupting the sex determination pathway in enteric neurons, Lgr3, or ovarian dILP8 prevents gut enlargement and reduces feeding. Thus, genetic sex establishes competence, steroid signalling primes it, and ovarian relaxin triggers it, defining a maternal intestinal plasticity checkpoint that ensures gut adaptations initiate only once reproduction is underway and energy demands peak. Our findings delineate an ovary-to-enteric-neuron axis that couples reproductive state to maternal gut plasticity.

physiology↗

Intersecting experimental evolution and CRISPR screens to identify novel insecticide resistance loci

Understanding toxin resistance in insects is key to appreciate niche adaptations but remains challenging due to its often-polygenic basis. A well-known example is the specialized association of Drosophila sechellia with noni fruit (Morinda citrifolia), which is toxic to most other insects, including the closely-related Drosophila simulans and Drosophila melanogaster. Toxicity of noni is due to its high concentration of octanoic acid (OA), but the mechanisms that determine sensitivity or resistance to OA in different species remain poorly understood. Here, we experimentally-evolved D. simulans with increased OA resistance, identifying multiple loci under selection. Cross-referencing these with a genome-wide, OA-resistance CRISPR screen in a D. melanogaster cell line highlighted two proteins: Kraken, a putative detoxification enzyme expressed in digestive and renal tissues, and Alkbh7, a mitochondrial protein linked to fatty acid metabolism. Both genes show elevated expression in D. sechellia and OA-resistant D. simulans. In D. melanogaster, kraken mutants are more OA-sensitive, while Alkbh7 overexpression increased OA resistance. Importantly, mutation of these genes in D. sechellia reduced OA tolerance. Our identification of genes underlying OA resistance in laboratory and natural contexts demonstrates how complementary, cross-species selection approaches can provide insights into complex mechanisms of toxin susceptibility and adaptation; such methods could also have practical applications in the characterization of natural and artificial insecticides.

evolutionary biology↗

Neuropeptide Dynamics Coordinate Layered Plasticity Mechanisms Adapting Drosophila Circadian Behavior to Changing Environment.

The Drosophila brain contains distinct sets of circadian oscillators responsible for generating the morning and evening bouts of locomotor activity, giving rise to a bimodal rest-activity pattern in light-dark cycles. We lack a mechanistic understanding of how environmental changes reshape this daily profile of rest-activity pattern. Here, we uncover a seasonal switch mechanism that remodels the evening bout of activity. Under summer-like conditions, an environment favored by fruit flies in temperate climates, levels of the PDF neuropeptide diminish, triggering a cascade. Lowered PDFR signaling disinhibits GSK3/SGG to advance the evening output. Upon sensing PDF loss, the neural activity weakens in the DN1p-SIFa circuit, responsible for promoting afternoon rest; leading to an earlier appearance of the evening peak. At the same time, the functional connections from DN1p to LNd oscillators strengthen, consequently handing over the evening pacemaker role to the DN1ps. Taken together, our findings elucidate how environment-induced changes in PDFR signaling tip the balanced output of the clock network, aligning daily rhythms with seasonal time. Neuropeptide-driven parallel adjustment of clock circuitry and clock protein functioning likely represents a conserved strategy across animal species, enabling them to adapt their daily behavior to seasonal changes throughout the year.

neuroscience↗