Biology subjects

Zanini, R.

Publications and source records attributed to Zanini, R..

3 recordsLinked to original sources

bioRxiv2025

Relaxin signaling is critical for virgin female reproductive physiology in Drosophila

Ovulation enables mature oocytes to exit the ovary for potential fertilization. In Drosophila, ovulation is induced by mating but also occurs spontaneously in virgins, with rates varying widely in natural populations: short oocyte retention is ancestral, while longer retention is favored in colder climates. The molecular regulation of spontaneous ovulation remains unclear. Here, we show that disrupting the relaxin/insulin-like peptide Dilp8 or its receptor Lgr3--an orthologue of vertebrate RXFP1/2--in follicle cells or specific neurons, respectively, delays ovulation, slows average egg transit time in the reproductive tract, and facilitates oogenesis progression beyond [~]2 mature oocytes per ovariole, leading to mature follicle accumulation in the ovary. Mating largely rescues these defects, suggesting the pathway is dispensable post-mating. Dilp8-Lgr3 signaling ensures high oocyte quality by promoting elimination of lower-quality aging oocytes and by antagonizing oogenesis progression via an undefined mechanism downstream of Lgr3+ neurons. Our findings provide a molecular basis for oocyte retention time regulation in Drosophila involving ovarian-nervous system cross-talk, and bring further support for an ancient, conserved role for relaxin-like signaling in regulating ovulation and overall female reproductive physiology. Summary statementThis study uncovers how ovary-neuron communication promotes spontaneous ovulation and prevents buildup of aging eggs, ensuring optimal egg quality in fruit flies.

physiology↗

bioRxiv2024

Neurogenetic evidence for oscillatory behavior of Lgr3-positive growth control interneurons in Drosophila

The ability to achieve a species-specific size and proportion despite developmental or environmental perturbations is termed developmental stability. The molecular and cellular processes behind this are best understood in insects. In Drosophila, a peripheral-tissue stress signal, the relaxin/insulin-like peptide Dilp8, promotes developmental stability during larval development via its neuronal receptor, Lgr3, an ortholog of vertebrate relaxin receptors. Lgr3 signaling is widely accepted to occur in-and to activate (depolarize)-the central brain growth-coordinating interneurons (PIL/GCL neurons). Here, using neurogenetic approaches, we confirm the requirement of Lgr3 in PIL/GCL neurons, but unexpectedly find that they require both silenced (hyperpolarized) and active (depolarized) states for an appropriate response to Dilp8. These results are most simply explained if Lgr3 activation by Dilp8 triggers PIL/GCL-neuron oscillatory activity, and such oscillations promote developmental stability. PIL/GCL neurons express and require Cyclin A-which can form cell-cycle oscillator complexes with cyclin-dependent kinases-for their response to Dilp8, independently of Rca1 (regulator of CycA)/Emi1 (early mitotic inhibitor). This opens the possibility that cell-cycle machinery can be co-opted for postmitotic neuron oscillations, adding to an increasing list of postmitotic roles for cyclins. Neuroanatomically, we show that PIL/GCL neurons form reciprocally-innervating loops, which are common architectures in oscillating circuits and central pattern generators. The role of PIL/GCL neurons in developmental stability mirrors other homeostasis-regulating, peptide-driven oscillatory circuits found in the vertebrate hypothalamus, a developmentally-homologous region to the one occupied by PIL/GCL neurons in the fly brain.

neuroscience↗

bioRxiv2024

Drosophila Glue Expulsion and Spreading Behavior is Modulated by Neuropeptidergic Mip-SPR Signaling from a Descending Command Neuron

At the end of their growth phase, Drosophila larvae remodel their bodies, firmly glue themselves to a substrate, and harden their cuticle in preparation for metamorphosis. This process is termed pupariation and it is triggered by a surge in the steroid hormone ecdysone. Substrate attachment is achieved by a recently-described pupariation subprogram called glue expulsion and spreading behavior (GSB). An epidermis-to-CNS Dilp8-Lgr3 relaxin signaling event that occurs downstream of ecdysone after pupariation initiation is critical for unlocking progression of the pupariation motor program towards GSB, but the factors and circuits acting downstream of Lgr3 signaling remain unknown. Here, we screened for such factors using cell type-specific RNA interference (RNAi) and behavioral monitoring. We identify Myoinhibiting peptide (Mip) and its highly conserved neuronal receptor, Sex peptide receptor (SPR), as a critical neuropeptidergic signaling pathway required to trigger and modulate multiple action components of GSB. In addition, we find that Mip is specifically required in a pair of descending neurons, whose optogenetic activation at a specific competence window triggers GSB-like behavior and whose neurogenetic silencing completely abrogates GSB without overtly affecting other pupariation components. This strongly suggests that these descending Mip neurons are developmentally-regulated GSB command neurons. Dissection of the GSB action components via muscle calcium-level monitoring coupled with cell-type specific RNAi indicates that Mip acts on multiple SPR-positive neuronal populations, which collectively define and pattern the sequence and timing of GSB actions. Hence, we have identified a pair of descending command neurons that utilize both synaptic transmission and neuropeptidergic signaling to trigger and modulate a complex innate behavior in Drosophila. Our results advance our molecular and cellular understanding of pupariation control, reveal the complexity of glue expulsion and spreading behavior control, provide insight into conserved aspects of Mip-SPR signaling in animals, and contribute to the understanding of how multi-step innate behaviors are coordinated in time and with other developmental processes through command neurons and neuropeptidergic signaling.

neuroscience↗