Ecdysis behavior in the tobacco hornworm Manduca sexta (Lepidoptera: Sphingidae) is triggered through reciprocal peptide signaling between the central nervous system and the epitracheal endocrine system. Recent evidence indicates that eclosion hormone may initiate endocrine events leading to ecdysis through its action on epitracheal glands to cause the release of ecdysis-triggering hormone (ETH). Direct exposure of epitracheal glands to eclosion hormone in vitro leads to secretion of ETH. The threshold concentration of eclosion hormone needed to evoke release of ETH is approximately 3 pmol l-1. Eclosion hormone also induces elevation of cyclic GMP, but not cAMP, concentration in epitracheal glands at concentrations similar to those causing release of ETH. Both cGMP and 8-Br-cGMP mimic the secretory action of eclosion hormone. The sensitivity of the secretory response to eclosion hormone occurs during a narrow window of development, beginning approximately 8 h prior to pupal ecdysis. However, eclosion hormone can cause elevation of cGMP levels in epitracheal glands long before they acquire competence to release ETH, showing that the initial portion of the signal transduction cascade is in place early in development, but that the absence of a downstream step in the cascade prevents secretion. Measurements of cGMP levels in epitracheal glands during the ecdysis sequence show a sudden elevation some 30 min after the onset of pre-ecdysis, well after ETH secretion has been initiated. ETH secretion can therefore be viewed as a two-step process, beginning at pre-ecdysis when cGMP levels are relatively low, followed by a massive release resulting from a logarithmic elevation of cGMP levels (Kingan, 1997).
At the end of each molt, insects shed the old cuticle by performing preecdysis and ecdysis behaviors. Regulation of these centrally patterned movements involves peptide signaling between endocrine Inka cells and the CNS. In Inka cells, the cDNA and gene encoding the Manduca sexta preecdysis-triggering hormone (PETH) and ecdysis-triggering hormone (ETH) that activate these behaviors, have been identified. Prior to behavioral onset, rising ecdysteroid levels induce expression of the ecdysone receptor (EcR) and ETH gene in Inka cells and evoke CNS sensitivity to PETH and ETH. Subsequent ecdysteroid decline is required for peptide release, which initiates three motor patterns in specific order: PETH triggers preecdysis I, while ETH activates preecdysis II and ecdysis. The Inka cell provides a model for linking steroid regulation of peptide hormone expression and release with activation of a defined behavioral sequence (Zitnan, 1999).
Three insect peptide hormones, eclosion hormone (EH), ecdysis-triggering hormone (ETH) and crustacean cardioactive peptide (see Drosophila Cardioacceleratory peptide), have been implicated in controlling ecdysis behavior in insects. This study examines the interactions among these three peptides in the regulation of the ecdysis sequence. Using intracellular recordings, it has been found that ETH is a potent activator of the EH neurons, causing spontaneous action potential firing, broadening of the action potential and an increase in spike peak amplitude. In turn, electrical stimulation of the EH neurons or bath application of EH to desheathed ganglia results in the elevation of cyclic GMP (cGMP) levels within the Cell 27/704 group (which contains CCAP). This cGMP production increases the excitability of these neurons, thereby facilitating CCAP release and the generation of the ecdysis motor program. Extracellular recordings from isolated nervous systems show that EH has no effect on nervous systems with an intact sheath. In desheathed preparations, in contrast, EH causes only the ecdysis motor output. The latency from EH application to ecdysis is longer than that after CCAP application, but shorter than that when ETH is applied to a whole central nervous system. These data support a model in which ETH causes pre-ecdysis behavior and at higher concentrations stimulates the EH neurons. EH release then facilitates the onset of ecdysis by enhancing the excitability of the CCAP neurons (Gammie, 1999).
Ecdysis, or molting behavior, in insects requires the sequential action of high levels of ecdysteroids, which induce accumulation of ecdysis-triggering hormone (ETH) in Inka cells, followed by low levels of ecdysteroids, permissive for the onset of the behavior. High ecdysteroid levels suppress the onset of the behavioral sequence by inhibiting the development of competence to secrete ETH. In pharate pupae of Manduca sexta, Inka cells in the epitracheal glands normally develop competence to secrete ETH in response to eclosion hormone (EH) 8 h before pupation. Injection of 20-hydroxyecdysone (20E) into precompetent insects prevents this acquisition of competence, but does not affect EH-evoked accumulation of the second messenger cyclic GMP. Precompetent glands acquire competence in vitro after overnight culture, and this can be prevented by the inclusion of 20E at concentrations greater than 0.1 microg ml(-1)in the culture medium. Actinomycin D completely inhibits the acquisition of competence, demonstrating that it is dependent on transcriptional events. Cultured epitracheal glands become refractory to the inhibitory effects of 20E in the acquisition of competence at least 3 h earlier than for Actinomycin D, indicating that 20E acts on an early step in a sequence of nuclear events leading to transcription of a structural gene. These findings suggest that declining ecdysteroid levels permit a late event in transcription, the product of which is downstream of EH receptor activation and cyclic GMP accumulation in the cascade leading to ETH secretion (Kingan, 2000).
Initiation of the ecdysis behavioral sequence in insects requires activation of the central nervous system (CNS) by pre-ecdysis-triggering hormone (PETH) and ecdysis-triggering hormone (ETH), which are released from the Inka cells of the epitracheal glands. The developmental events preceding larval and pupal ecdysis of Manduca sexta involve a dual action of ecdysteroids on the epitracheal glands and CNS. The low steroid levels in freshly ecdysed and feeding larvae are associated with small-sized epitracheal glands, reduced peptide production in Inka cells and insensitivity of the CNS to ETH. The elevated ecdysteroid levels before each ecdysis led to a dramatic enlargement of Inka cells and increased production of peptide hormones and their precursors. As blood ecdysteroids reach peak levels, the CNS becomes responsive to Inka cell peptides. These effects of natural ecdysteroid pulses can be experimentally induced by injection of 20-hydroxyecdysone or the ecdysteroid agonist tebufenozide (RH-5992) into ecdysed larvae, thus stimulating peptide production in Inka cells and inducing CNS sensitivity to ETH. A direct steroid action on the CNS is demonstrated by subsequent treatment of isolated nerve cords from ecdysed larvae with 20-hydroxyecdysone and ETH, which results in pre-ecdysis or ecdysis bursts. These data show that ecdysteroid-induced transcriptional activity in both the epitracheal glands and the CNS are necessary events for the initiation of the ecdysis behavioral sequence (Zitnanova, 2001).
Inka cells of the epitracheal endocrine system produce peptide hormones involved in the regulation of insect ecdysis. In the silkworm Bombyx mori, injection of Inka cell extract into pharate larvae, pupae or adults activates the ecdysis behavioral sequence. In the present study, the identification is reported of three peptides in these extracts, pre-ecdysis-triggering hormone (PETH), ecdysis-triggering hormone (ETH) and ETH-associated peptide (ETH-AP); these are encoded by the same cDNA precursor. Strong immunoreactivity associated with each peptide in Inka cells prior to ecdysis disappears during each ecdysis, indicating complete release of these peptides. Injection of either PETH or ETH alone is sufficient to elicit the entire ecdysis behavioral sequence through the direct action on abdominal ganglia; cephalic and thoracic ganglia are not required for the transition from pre-ecdysis to ecdysis behavior. In vitro data provide evidence that these peptides control the entire ecdysis behavioral sequence through activation of specific circuits in the nervous system. Ecdysis of intact larvae is associated with the central release of eclosion hormone (EH) and elevation of cyclic 3',5'-guanosine monophosphate (cGMP) in the ventral nerve cord. However, injection of ETH into isolated abdomens induces cGMP elevation and ecdysis behavior without a detectable release of EH, suggesting that an additional central factor(s) may be involved in the activation of this process. These findings provide the first detailed account of the natural and hormonally induced behavioral sequence preceding larval, pupal and adult ecdyses of B. mori and highlight significant differences in the neuro-endocrine activation of pre-ecdysis and ecdysis behaviors compared with the related moth, Manduca sexta (Zitnan, 2002).
The sequential behaviors shown by insects at ecdysis are due to the sequential release of various hormones, but the transition from one phase to the next can be fine-tuned by inhibitory influences. The ecdysis sequence in the moth Manduca sexta was initiated by injecting sensitive animals with the neuropeptide ecdysis-triggering hormone (ETH). Exposure to ETH stimulates the release of eclosion hormone (EH) which, in turn, activates a set of neurons containing crustacean cardioactive peptide (CCAP) by elevating their levels of intracellular cyclic GMP. This study characterizes a set of non-CCAP containing neurons that also appear to be EH targets because of their response to cyclic GMP at ecdysis. The neurons did not display leucokinin-, diuretic-hormone- or FMRFamide-like immunoreactivity. They are probably bursicon-containing cells. After release of EH, there is a transient inhibition of the abdominal centers responsible for ecdysis. Transection experiments suggest that this suppression is via descending inhibitory units from the suboesophageal and thoracic ganglia. The duration of this inhibition appears to depend on the levels of cyclic GMP and can be extended by pharmacologically suppressing cyclic GMP breakdown. Brief exposure to CO2 causes premature ecdysis. Since the CO2 treatment is effective only after EH release, it probably acts by suppressing descending inhibition. Studies on adult eclosion suggest that CO2, given at the appropriate time, can uncouple the basic larval motor program from modulatory influences provided by the adult pterothoracic ganglion. CO2 therefore appears to be a novel and non-invasive tool for studies of ecdysis behavior in insects (Fuse, 2002).
Pre-ecdysis- and ecdysis-triggering hormones (PETH and ETH) from endocrine Inka cells initiate ecdysis in moths and Drosophila through direct actions on the central nervous system (CNS). Using immunohistochemistry, Inka cells were found in representatives of all major insect orders. In most insects, Inka cells are numerous, small and scattered throughout the tracheal system. Only some higher holometabolous insects exhibit 8-9 pairs of large Inka cells attached to tracheae in each prothoracic and abdominal segment. The number and morphology of Inka cells can be very variable even in the same individuals or related insects, but all produce peptide hormones that are completely released at each ecdysis. Injection of tracheal extracts prepared from representatives of several insect orders induces pre-ecdysis and ecdysis behaviors in pharate larvae of Bombyx, indicating functional similarity of these peptides. Several PETH-immunoreactive peptides were isolated from tracheal extracts of the cockroach Nauphoeta cinerea and the bug Pyrrhocoris apterus and the gene encoding two putative ETHs were identified in the mosquito Anopheles gambiae. Inka cells also stain with antisera to myomodulin, FMRFamide and other peptides sharing RXamide carboxyl termini. However, enzyme immunoassays show that these antisera cross-react with PETH and ETH. These results suggest that Inka cells of different insects produce only peptide hormones closely related to PETH and ETH, which are essential endocrine factors required for activation of the ecdysis behavioral sequence (Zitnan, 2003).
At the end of each developmental stage, insects perform the ecdysis sequence, an innate behavior necessary for shedding the old cuticle. Ecdysis triggering hormones (ETHs) initiate these behaviors through direct actions on the CNS. This study identifies the ETH receptor (ETHR) gene in the moth Manduca sexta; the gene encodes two subtypes of GPCR (ETHR-A and ETHR-B). Expression of ETHRs in the CNS coincides precisely with acquisition of CNS sensitivity to ETHs and behavioral competence. ETHR-A occurs in diverse networks of neurons, producing both excitatory and inhibitory neuropeptides, which appear to be downstream signals for behavior regulation. These peptides include allatostatins, crustacean cardioactive peptide (CCAP), calcitonin-like diuretic hormone, CRF-like diuretic hormones (DHs) 41 and 30, eclosion hormone, kinins, myoinhibitory peptides (MIPs), neuropeptide F, and short neuropeptide F. In particular, cells L3,4 in abdominal ganglia coexpress kinins, DH41, and DH30, which together elicit the fictive preecdysis rhythm. Neurons IN704 in abdominal ganglia coexpress CCAP and MIPs, whose joint actions initiate the ecdysis motor program. ETHR-A also is expressed in brain ventromedial cells, whose release of EH increases excitability in CCAP/MIP neurons. These findings provide insights into how innate, centrally patterned behaviors can be orchestrated via recruitment of peptide cotransmitter neurons (Kim, 2006b).
In M. sexta, the shedding of old cuticle is accomplished by the ecdysis sequence consisting of the sequential behaviors preecdysis I, preecdysis II, and ecdysis. Each individual motor program is triggered by direct actions of PETH and ETH on the CNS. The ecdysis sequence is initiated by corazonin release from the brain, causing low-level secretion of pre-ecdysis triggering hormone (PETH) and ETH from Inka cells. These initial low levels of circulating peptides activate the ETHR-A in abdominal neurons L3,4 to induce preecdysis I through central release of DHs and kinins. At the same time, ETH acts on unidentified neurons (possibly expressing ETHR-B) to activate preecdysis II and specific ETHR-A neurons in the entire CNS to activate the ecdysis network. This ETHR-A network includes EH-producing VM neurons and IN704 in the AG1–7, which produce CCAP and MIPs. Activation of the ecdysis network is indicated by EH-mediated cGMP elevation in abdominal neurons ~30 min after onset of preecdysis I. However, descending inhibitory neurons (possibly expressing ETHR-B) in the subesophageal ganglia and TG1–3 suppress the release of CCAP and MIPs from IN704 and delay ecdysis onset. The switch from preecdysis to ecdysis is mediated by central release of CCAP and MIPs from IN704. CCAP apparently plays an excitatory role in this process and controls ecdysis execution, whereas MIPs appear to inhibit activities of other neurons not involved in ecdysis. Finally, bursicon and CCAP are released from cells 27 (NS27) to control postecdysis behaviors: cuticle expansion, hardening, and tanning. Physiological roles of other identified ETHR-A neurons expressing various neuropeptides (e.g., NPF, small NPF/MIPs, and calcitonin-like DH/MIPs) are not clear, and their functional analysis is in progress (Kim, 2006b).
It is well established that peptidergic inputs modulate central pattern generators. In the case of the crustacean stomatogastric ganglion, peptides alter the synaptic strength and intrinsic properties of neurons within the ganglion, resulting in different versions of pyloric and gastric mill rhythms. Similar regulatory mechanisms may operate for the ecdysis sequence, whereby sequential release of neuropeptides reconfigures the activity of multiple central pattern generators in succession (Kim, 2006b).
In this study, it was discovered that numerous central peptidergic ensembles express ETHRs and, consequently, are likely primary targets of ETH. Peptides produced by these ensembles are prime candidates for downstream signals in the recruitment of each centrally patterned phase of the ecdysis sequence. Possible roles of two specific peptidergic ensembles have been shown: a neuropeptide mixture consisting of DHs and kinins produced by abdominal L3,4 neurons generates the preecdysis I rhythm, whereas a combination of CCAP and MIPs produced by IN704 neurons elicits the ecdysis rhythm (Kim, 2006b).
In related work, it has been shown that ensembles of neurons in D. melanogaster homologous to those in M. sexta (EH-containing VM neurons, CCAP/MIPs-containing IN704 neurons, and CCAP/bursicon-containing NS27 neurons) become active at the onset of successive behavioral subunits (Kim, 2006a). Taken together, these findings indicate that sequential recruitment of peptidergic ensembles elicits components of an innate behavior in stepwise fashion. It seems reasonable to suggest that central neuropeptide release as described here may represent a general mechanism for orchestration of behaviors (Kim, 2006b).
Ecdysis behavior in arthropods is driven by complex interactions among multiple neuropeptide signaling systems. To understand the roles of neuropeptides and their receptors in the red flour beetle, Tribolium castaneum, systemic RNA interference (RNAi) experiments were performed utilizing post-embryonic injections of double-stranded (ds) RNAs corresponding to ten gene products representing four different peptide signaling pathways: eclosion hormone (EH), ecdysis triggering hormone (ETH), crustacean cardioactive peptide (CCAP) and bursicon. Behavioral deficiencies and developmental arrests occurred as follows: RNAi of (1) eh or eth disrupted preecdysis behavior and prevented subsequent ecdysis behavior; (2) ccap interrupted ecdysis behavior; and (3) bursicon subunits resulted in wrinkled elytra due to incomplete wing expansion, but there was no effect on cuticle tanning or viability. RNAi of genes encoding receptors for those peptides produced phenocopies comparable to those of their respective cognate neuropeptides, except in those cases where more than one receptor was identified. The phenotypes resulting from neuropeptide RNAi in Tribolium differ substantially from phenotypes of the respective Drosophila mutants. Results from this study suggest that the functions of neuropeptidergic systems that drive innate ecdysis behavior have undergone significant changes during the evolution of arthropods (Arakane, 2008).
The earliest peptide signal for ecdysis behavior in Manduca so far identified is corazonin, which triggers the neuroendocrine cascade by inducing the release of ETH from the epitracheal glands. However, in Tribolium and also in other coleopteran species, corazonin is apparently absent because there has been no report of immunoreactivity with corazonin antiserum. Furthermore, no Tribolium sequences encoding this peptide or its receptor have been reported so far. Thus, the signal initiating ecdysis in this coleopteran must be something other than corazonin. In the case of the albino locust, which is believed to lack corazonin, there is no ecdysis deficiency reported, implying that corazonin may be lepidopteran-specific as a signal for ETH release (Arakane, 2008).
Severe deficiencies in preecdysis behavior were observed in Tribolium after treatment with either dseh, dseth, dsethr or dsethr-a. There were some occasional twitching-like D–V contractions in these insects, which may have been caused by incomplete suppression of the targeted mRNA. This deficiency in preecdysis behavior resulted in the failure of subsequent ecdysis behavior, which in turn resulted in failure to eclose and finally in death. The ETH signal has been found to be necessary and sufficient in Drosophila for both preecdysis and ecdysis behaviors. In Manduca, the sufficiency of ETH for inducing premature preecdysis and ecdysis behaviors also supports the conclusion that ETH is one of the earliest ecdysis-initiating molecules. This study also supports the notion of ETH being an early essential signal for ecdysis in Tribolium. In addition, dseth was found to cause deficiencies in larval and pupal ecdysis depending on the time of injection (Arakane, 2008).
Two subtypes of ETH receptors, A and B, arising from mutually exclusive alternative exon usage, are highly conserved in insects. Studies with Manduca and Drosophila showed that ethr-a is expressed mainly in numerous peptidergic cells in the CNS, while ethr-b is expressed in poorly-characterized interneuron cells. Exon-specific dsRNA in Tribolium showed that dsethr-a-treated insects had significantly fewer D–V contractions, a phenotype identical to that obtained following treatment with dseth or dseh. However, eclosion of insects injected with dsethr-b occurred normally, with no substantial reduction in preecdysial D–V contractions. Therefore, ethr-a, which activates downstream peptidergic signals, is a necessary component in Tribolium eclosion, whereas the role of ethr-b remains unclear. Switching from one behavior to the next within a certain time interval in the behavioral sequence had been thought to involve inhibitory neurons, it was not possible to determine whether premature ecdysis behavior occurred in the dsethr-b-injected Tribolium as a result of defects in inhibitory neurons (Arakane, 2008).
Positive feedback between EH and ETH has been found in Manduca. Release of ETH is triggered by corazonin as the initiator of the EH-ETH feedback loop. EH-associated positive feedback induces a massive release of ETH for the initiation of ecdysis motor patterns. However, a positive feedback loop was not found in Drosophila. Rather, Drosophila EH apparently acts downstream of ETH and is the factor triggering ecdysis behavior, a conclusion based on the timing of the cellular response of EH cells, which show Ca2+ elevation upon treatment with ETH during pupal ecdysis. Surprisingly, the EH-cell-knockout in Drosophila resulted in only a partial impairment during adult eclosion, with a significant proportion of the insects dying before pupation. In Tribolium, EH was required for early preecdysis behavior. Thus, the ETH-EH feedback loop, if it occurs, probably occurs during preecdysis in Tribolium, as it does in Manduca (Arakane, 2008).
In Drosophila, the ccap null mutant did not show any abnormality during development or ecdysis, whereas ccap-cell ablation resulted in deficiencies in both pupal and adult ecdysis. Therefore, it was concluded that other neuropeptides, which are co-expressed in the CCAP cells, are probably responsible for the phenotypes of the ccap cell-knockout. Thus, the role of CCAP in Drosophila ecdysis remains unclear. The neuropeptides co-expressed in the CCAP cells with presumed functions in ecdysis are bursicon, partner of bursicon and myoinhibitory peptide (Arakane, 2008).
In contrast to Drosophila, ccap RNAi in Tribolium resulted in a lethal arrest during ecdysis. The ecdysis deficiency was associated with significantly weaker behaviors, including reverse-bending, wing air-filling and A–P contraction, whereas these insects underwent normal preecdysis behavior. The dsccapr-2 treatment resulted in the same phenotype as that of dsccap, whereas dsccapr-1 treatment did not produce any abnormalities. Therefore, CCAP and CCAPR-2 are in the signaling pathway for ecdysis behavior, while the function of CCAPR-1 remains unknown (Arakane, 2008).
The bur and pbur genes in Tribolium form a tandem pair in the genome, separated by only ~1.3 kb. This arrangement is similar to the bur/pbur gene structure in the honeybee. Previously, it was proposed that the honeybee bur/pbur gene consisted of one long open reading frame encoding a multi-domain protein including both bur and pbur. Subsequently, however, different transcription units for bur and pbur were reported. Using RT-PCR this study determined that Tribolium bur and pbur are probably separate transcription units. Results from gene-specific RNAi for both bur and pbur support the hypothesis that two different transcription units exist. In addition, whereas mosquito bur was found to undergo trans-splicing, this study found that the Tribolium bur and pbur genes contain complete open reading frames, excluding the possibility of trans-splicing (Arakane, 2008).
A heterodimeric complex Bur/pBur consisting of the products of the bur and pbur genes is a cysteine knot family hormone that has been reported to initiate two different functional activities in Drosophila, namely cuticle tanning and wing expansion after adult eclosion. Drosophila mutants for bur and receptor mutant rickets (rk) showed deficiencies in both tanning and wing expansion (Arakane, 2008).
This study discovered that treatments with dsbur, dspbur or dsrk all produced similar postecdysis defects, namely weak postecdysis activity, wrinkled elytra and a failure to retract the hindwing, but none of these caused lethality within the observation time of 2–3 weeks after eclosion. In Drosophila, bursicon induces wing cell death and wing expansion after eclosion. The wrinkled elytra and the deficiency in proper folding of the hindwing after RNAi in Tribolium may be equivalent to the Drosophila phenotype. Interestingly, RNAi of these genes resulted in significantly diminished strengths in preecdysis behavior. The data imply that bur/pbur and their putative receptor rk in Tribolium are involved in the regulation of preecdysis behavior, and even more in postecdysis behavior. An additional unique phenotype was found only in insects injected with dsbur, which exhibited weaker A–P contractions during ecdysis and consequently an extended duration for completion of the shedding of the exuvium. These observations suggest an unknown but separate function for bursicon in addition to its role as a component of dimeric Bur/pBur acting through its receptor Rickets. Alternatively, the phenotypic variation could have been caused by different dosages of remaining transcripts in RNAi or by stability of the protein that had been produced earlier (Arakane, 2008).
Perhaps the most interesting observation in this study is that normal tanning occurs in beetles subjected to RNAi for the group of genes encoding the neuropeptides described in this study. Maturation of the cuticle is a gradual process of pigmentation and sclerotization during the first five days after eclosion. A recent study involving Drosophila has shown that bursicon acts through phosphorylation of tyrosine hydroxylase, which catalyzes an early step of catecholamine production for cuticle tanning. It has been shown previously that RNAi of Tribolium laccase 2, which is a phenoloxidase downstream of tyrosine hydroxylase in the same metabolic pathway, suppressed cuticle tanning. This result indicated that a similar cuticle tanning pathway exists in both Drosophila and Tribolium. It is concluded, therefore, that the Bur/pBur signaling pathway is required for proper wing expansion and folding in Tribolium but not for tyrosine hydroxylase/laccase-mediated tanning. Recent study in the silkworm also reported that RNAi of bur found no distinct tanning phenotype, while a deficiency in wing expansion was observed. In addition, the regulation of cuticle tanning in Tribolium appears to be different from that of Drosophila, even though the tanning pathway itself is probably conserved (Arakane, 2008).
This has been a study of key peptidergic signaling systems for insect ecdysis in T. castaneum, representing a more basal holometabolous order (Coleoptera) relative to the species of Lepidoptera and Diptera studied previously. RNAi in Tribolium followed by behavioral analysis revealed differences in the roles of EH, CCAP and bursicon compared to those found in Drosophila. Both ETH and EH are necessary for preecdysis and ecdysis behaviors in Tribolium, while an essential role of EH has not been found in Drosophila. CCAP is necessary for ecdysis behavior in Tribolium, whereas the Drosophila ccap null mutant shows normal ecdysis. In Tribolium Bur/pBur is necessary for postecdysis behavior, including wing expansion and folding, whereas, unlike the case in dipterans, it does not have a role in cuticle tanning (Arakane, 2008). Bur/pBur signaling is involved in preecdysis behavior. Only bursicon appears to have an additional role in ecdysis behavior in Tribolium (Arakane, 2008).
The differences in the precise roles of each peptidergic component among Tribolium, Drosophila and Manduca in controlling innate ecdysis behavior and cuticle tanning can be interpreted as a consequence of evolution. The loss of essential roles for EH and CCAP as well as a gain in function for bursicon in Drosophila may be associated with modifications of the requirements of those neuropeptidergic signals in these processes, whereas the more ancestral Tribolium and possibly Manduca strictly require EH and CCAP signaling systems. A comparative analysis of the functions of peptidergic signals from additional taxa will provide further insights into the evolution and regulation of ecdysis and tanning in the Ecdysozoa (Arakane, 2008).
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