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The insect molting process is critical to growth and development and is regulated in part by the neuropeptides corazonin, eclosion hormone, and α and β bursicon. We found messages in a synganglion transcriptome from adult, female American dog ticks, Dermacentor variabilis (that do not molt), with a high similarity to the larval insect neuropeptides that control molting. The phylogenetic analysis of the tick putative neuropeptides compared to other arthropods is discussed in detail. The relative gene expression of these peptides was determined by quantitative PCR during the following adult developmental stages: (i) virgin, unfed 0–24 h after entering the adult stage (non-host-seeking), (ii) host-seeking, unfed, and not mated (3 d after emergence), (iii) part-fed (unmated, attached to host; 1st and 3rd day after emergence), (iv) mated (females are part-fed; allowed to mate for ≤1 day, 7th day after emergence), (v) mated repletes (completion of blood feeding but still attached to host), and (vi) post-drop-off (from host) with egg laying starting within 1 d of detachment. Eclosion hormone transcript levels peaked at mating and at drop-off. Bursicon α levels were highest just after molting into adults, with a second smaller peak in replete females. Bursicon β levels were highest (32-fold) post-drop-off. Corazonin message levels peaked in part-feds and were much higher (40-fold) in repletes compared to 0–24 h after emergence. RNAi suppression of the corazonin message by injection in newly molted ticks reduced oviposition and the number of vitellogenic eggs in the ovaries at drop-off but had no apparent effect on host-seeking, partial feeding, mating, feeding to repletion, and drop-off. The possible roles of these transcripts in adult, female tick development are discussed.

Seasonal polyphenism enables organisms to adapt to environmental challenges by increasing phenotypic diversity. Cacopsylla chinensis exhibits remarkable seasonal polyphenism, specifically in the form of summer-form and winter-form, which have distinct morphological phenotypes. Previous research has shown that low temperature and the temperature receptor CcTRPM regulate the transition from summer-form to winter-form in C. chinensis by impacting cuticle content and thickness. However, the underling neuroendocrine regulatory mechanism remains largely unknown. Bursicon, also known as the tanning hormone, is responsible for the hardening and darkening of the insect cuticle. In this study, we report for the first time on the novel function of Bursicon and its receptor in the transition from summer-form to winter-form in C. chinensis . Firstly, we identified CcBurs-α and CcBurs-β as two typical subunits of Bursicon in C. chinensis , which were regulated by low temperature (10 °C) and CcTRPM . Subsequently, CcBurs-α and CcBurs-β formed a heterodimer that mediated the transition from summer-form to winter-form by influencing the cuticle chitin contents and cuticle thickness. Furthermore, we demonstrated that CcBurs-R acts as the Bursicon receptor and plays a critical role in the up-stream signaling of the chitin biosynthesis pathway, regulating the transition from summer-form to winter-form. Finally, we discovered that miR-6012 directly targets CcBurs-R , contributing to the regulation of Bursicon signaling in the seasonal polyphenism of C. chinensis . In summary, these findings reveal the novel function of the neuroendocrine regulatory mechanism underlying seasonal polyphenism and provide critical insights into the insect Bursicon and its receptor. A bug known as pear psylla is a common pest on pear trees in China and other East Asian countries. It feeds off the sap of young leaves and shoots, causing damage to the trees and decreasing the amount of fruit they produce. To survive all-year round, pear psylla changes its body between distinct summer- and winter-forms, a phenomenon known as seasonal polyphenism. In winter, cooler temperatures trigger young pear psylla to darken and thicken the protective cuticle layer coating their bodies. However, the mechanisms behind this seasonal transformation are not fully understood. One possible regulator of this process is the hormone Bursicon which is known to control cuticle development in juvenile insects. The hormone has two subunits that join to form dimers, which then activate specific receptors that initiate signaling pathways within the insect’s body. Here, Zhang et al. used molecular biology and genetic techniques to study the role of Bursicon dimers in seasonal polyphenism in pear psylla. Bursicon can assemble either as a homodimer (made up of two identical subunits), or a heterodimer (made up two different subunits). Zhang et al. found that low temperatures triggered the formation of both homodimers and heterodimers of Bursicon. However, only the heterodimers activated a receptor, called CcBurs-R , which enabled the pear psylla to transition into their winter-form. The team also identified a small molecule called a micro RNA that regulates this switch by decreasing the production of the CcBurs-R receptor. The findings by Zhang et al. advance our understanding of how seasonal polyphenism operates in pear psylla. Many other insects display seasonal polyphenism, and further research could reveal whether Bursicon plays a similar regulatory role across different species.

(1) Background: Global climate change is intensifying, and the vigorous development and utilization of saline–alkali land is of great significance. As an important economic aquatic species in the context of saline–alkali aquaculture, it is highly significant to explore the regulatory mechanisms of Eriocheir sinensis under alkaline conditions. In particular, the brain (cerebral ganglion for crustaceans) serves as a vital regulatory organ in response to environmental stress; (2) Methods: In this study, a comparative transcriptome approach was employed to investigate the key regulatory genes and molecular regulatory mechanisms in the cerebral ganglion of E. sinensis under alkaline stress. (3) Results: The results demonstrated that the cerebral ganglion of E. sinensis exhibited a positive response to acute alkaline stress. Pathways associated with signal transduction and substance transportation, such as “phagosome” and “regulation of actin cytoskeleton”, along with regulatory genes involved in antioxidation, were upregulated synergistically to maintain homeostasis under alkaline stress. Furthermore, it was discovered for the first time that bursicon plays a positive regulatory role in the adaptation of E. sinensis to alkalinity. (4) Conclusions: The present study elucidates the molecular regulatory pattern of the cerebral ganglion in E. sinensis under acute alkaline stress as well as revealing a novel role of bursicon in facilitating adaptation to alkalinity in E. sinensis, providing valuable theoretical insights into the molecular regulatory mechanisms underlying the responses of cerebral ganglia to saline–alkali environments. These findings also offer a theoretical reference for promoting the sustainable development of the E. sinensis breeding industry under saline–alkali conditions.

Identifying neural substrates of behavior requires defining actions in terms that map onto brain activity. Brain and muscle activity naturally correlate via the output of motor neurons, but apart from simple movements it has been difficult to define behavior in terms of muscle contractions. By mapping the musculature of the pupal fruit fly and comprehensively imaging muscle activation at single-cell resolution, we here describe a multiphasic behavioral sequence in Drosophila . Our characterization identifies a previously undescribed behavioral phase and permits extraction of major movements by a convolutional neural network. We deconstruct movements into a syllabary of co-active muscles and identify specific syllables that are sensitive to neuromodulatory manipulations. We find that muscle activity shows considerable variability, with sequential increases in stereotypy dependent upon neuromodulation. Our work provides a platform for studying whole-animal behavior, quantifying its variability across multiple spatiotemporal scales, and analyzing its neuromodulatory regulation at cellular resolution. How do we find out how the brain works? One way is to use imaging techniques to visualise an animal’s brain in action as it performs simple behaviours: as the animal moves, parts of its brain light up under the microscope. For laboratory animals like fruit flies, which have relatively small brains, this lets us observe their brain activity right down to the level of individual brain cells. The brain directs movements via collective activity of the body’s muscles. Our ability to track the activity of individual muscles is, however, more limited than our ability to observe single brain cells: even modern imaging technology still cannot monitor the activity of all the muscle cells in an animal’s body as it moves about. Yet this is precisely the information that scientists need to fully understand how the brain generates behaviour. Fruit flies perform specific behaviours at certain stages of their life cycle. When the fly pupa begins to metamorphose into an adult insect, it performs a fixed sequence of movements involving a set number of muscles, which is called the pupal ecdysis sequence. This initial movement sequence and the rest of metamorphosis both occur within the confines of the pupal case, which is a small, hardened shell surrounding the whole animal. Elliott et al. set out to determine if the fruit fly pupa’s ecdysis sequence could be used as a kind of model, to describe a simple behaviour at the level of individual muscles. Imaging experiments used fly pupae that were genetically engineered to produce an activity-dependent fluorescent protein in their muscle cells. Pupal cases were treated with a chemical to make them transparent, allowing easy observation of their visually ‘labelled’ muscles. This yielded a near-complete record of muscle activity during metamorphosis. Initially, individual muscles became active in small groups. The groups then synchronised with each other over the different regions of the pupa’s body to form distinct movements, much as syllables join to form words. This synchronisation was key to progression through metamorphosis and was co-ordinated at each step by specialised nerve cells that produce or respond to specific hormones. These results reveal how the brain might direct muscle activity to produce movement patterns. In the future, Elliott et al. hope to compare data on muscle activity with comprehensive records of brain cell activity, to shed new light on how the brain, muscles, and other factors work together to control behaviour.

Activation of caspases is an essential step toward initiating apoptotic cell death. During metamorphosis of Drosophila melanogaster, many larval neurons are programmed for elimination to establish an adult central nervous system (CNS) as well as peripheral nervous system (PNS). However, their neuronal functions have remained mostly unknown due to the lack of proper tools to identify them. To obtain detailed information about the neurochemical phenotypes of the doomed larval neurons and their timing of death, we generated a new GFP-based caspase sensor (Casor) that is designed to change its subcellular position from the cell membrane to the nucleus following proteolytic cleavage by active caspases. Ectopic expression of Casor in vCrz and bursicon, two different peptidergic neuronal groups that had been well-characterized for their metamorphic programmed cell death, showed clear nuclear translocation of Casor in a caspase-dependent manner before their death. We found similar events in some cholinergic neurons from both CNS and PNS. Moreover, Casor also reported significant caspase activities in the ventral and dorsal common excitatory larval motoneurons shortly after puparium formation. These motoneurons were previously unknown for their apoptotic fate. Unlike the events seen in the neurons, expression of Casor in non-neuronal cell types, such as glial cells and S2 cells, resulted in the formation of cytoplasmic aggregates, preventing its use as a caspase sensor in these cell types. Nonetheless, our results support Casor as a valuable molecular tool not only for identifying novel groups of neurons that become caspase-active during metamorphosis but also for monitoring developmental timing and cytological changes within the dying neurons.

During development, HOX genes play critical roles in the establishment of segmental differences. In the Drosophila central nervous system, these differences are manifested in the number and type of neurons generated by each neuroblast in each segment. HOX genes can act either in neuroblasts or in postmitotic cells, and either early or late in a lineage. Additionally, they can be continuously required during development or just at a specific stage. Moreover, these features are generally segment-specific. Lately, it has been shown that contrary to what happens in other tissues, where HOX genes define domains of expression, these genes are expressed in individual cells as part of the combinatorial codes involved in cell type specification. In this report we analyse the role of the Bithorax-complex genes – Ultrabithorax, abdominal-A and Abdominal-B – in sculpting the pattern of crustacean cardioactive peptide (CCAP)-expressing neurons. These neurons are widespread in invertebrates, express CCAP, Bursicon and MIP neuropeptides and play major roles in controlling ecdysis. There are two types of CCAP neuron: interneurons and efferent neurons. Our results indicate that Ultrabithorax and Abdominal-A are not necessary for specification of the CCAP-interneurons, but are absolutely required to prevent the death by apoptosis of the CCAP-efferent neurons. Furthermore, Abdominal-B controls by repression the temporal onset of neuropeptide expression in a subset of CCAP-efferent neurons, and a peak of ecdysone hormone at the end of larval life counteracts this repression. Thus, Bithorax complex genes control the developmental appearance of these neuropeptides both temporally and spatially.

Following eclosion from the pupal case, wings of the immature adult fly unfold and expand to present a flat wing blade. During expansion the epithelia, which earlier produced the wing cuticle, delaminate from the cuticle, and the epithelial cells undergo an epithelial–mesenchymal transition (EMT). The resulting fibroblast-like cells then initiate a programmed cell death, produce an extracellular matrix that bonds dorsal and ventral wing cuticles, and exit the wing. Mutants that block wing expansion cause persistence of intact epithelia within the unexpanded wing. However, the normal progression of chromatin condensation and fragmentation accompanying programmed cell death in these cells proceeds with an approximately normal time course. These observations establish that the Bursicon/Rickets signaling pathway is necessary for both wing expansion and initiation of the EMT that leads to removal of the epithelial cells from the wing. They demonstrate that a different signal can be used to activate programmed cell death and show that two distinct genetic programs are in progress in these cells during wing maturation.

Peptidergic neurons are not easily integrated into current connectomics concepts, since their peptide messages can be distributed via non-synaptic paracrine signaling or volume transmission. Moreover, the polarity of peptidergic interneurons in terms of in- and out-put sites can be hard to predict and is very little explored. We describe in detail the morphology and the subcellular distribution of fluorescent vesicle/dendrite markers in CCAP neurons (NCCAP), a well defined set of peptidergic neurons in the Drosophila larva. NCCAP can be divided into five morphologically distinct subsets. In contrast to other subsets, serial homologous interneurons in the ventral ganglion show a mixed localization of in- and output markers along ventral neurites that defy a classification as dendritic or axonal compartments. Ultrastructurally, these neurites contain both pre- and postsynaptic sites preferably at varicosities. A significant portion of the synaptic events are due to reciprocal synapses. Peptides are mostly non-synaptically or parasynaptically released, and dense-core vesicles and synaptic vesicle pools are typically well separated. The responsiveness of the NCCAP to ecdysis-triggering hormone may be at least partly dependent on a tonic synaptic inhibition, and is independent of ecdysteroids. Our results reveal a remarkable variety and complexity of local synaptic circuitry within a chemically defined set of peptidergic neurons. Synaptic transmitter signaling as well as peptidergic paracrine signaling and volume transmission from varicosities can be main signaling modes of peptidergic interneurons depending on the subcellular region. The possibility of region-specific variable signaling modes should be taken into account in connectomic studies that aim to dissect the circuitry underlying insect behavior and physiology, in which peptidergic neurons act as important regulators.

Soon after eclosion, epithelial cells of the Drosophila wing undergo a number of the processes due to a release of the neurohormone bursicon and its further binding to the GPCR Rickets, collectively referred to as wing maturation. Here we propose hypothetical models of the interaction between extracellular Miniature, and also Dusky, proteins and proteins responsible for triggering of the wing maturation processes in