ライフサイエンスコーパス: sting

1 e (cGAS) and stimulator of interferon genes (STING).

2 eam adaptor protein stimulator of IFN genes (STING).

3 ER) adapter, stimulator of interferon genes (STING).

4 ves TLR9, AIM2, and stimulator of IFN genes (STING).

5 rs bind directly to stimulator of IFN genes (STING).

6 eaction following a honeybee, vespid, or ant sting.

7 via a route different from that of jellyfish sting.

8 e expression, albeit to a lesser extent than STING.

9 tivation, have differential requirements for STING.

10 at the Golgi is essential for activation of STING.

11 human and murine hepatocytes do not express STING.

12 ts for murine (DMXAA) or human (2',3'-cGAMP) STING.

13 hrough a pathway dependent on the DNA sensor STING.

14 nteractions between HSV-1 and the DNA sensor STING.

15 nger cGAMP to activate the signaling adaptor STING.

16 immunity dependent on the adaptors MAVS and STING.

17 DNA sensor cGAS and its downstream effector STING.

18 se cGAS and the cyclic dinucleotide receptor STING.

19 protein interacts with and colocalizes with STING.

20 at relies on the immunosuppressive action of STING.

21 rkers to predict tolerance to bee and vespid stings.

22 ients with systemic reactions to Hymenoptera stings.

23 ghtly but significantly fewer barbs on their stings (-7% in the 40K-treated bees).

24 Therefore, STING, a critical innate sensor, also functions intrinsi

25 In the LLC model, STING ablation enhanced CD8(+) T-cell infiltration and t

26 the cyclic GMP-AMP synthase, which generates STING-activating cyclic dinucleotides after binding cyto

27 We describe novel STING-activating cyclic dinucleotides whose constituent

28 The STING-activating nanovaccine offers a simple, safe and r

29 2'3'-cGAMP acts as a second messenger for STING activation and triggers TBK1/IRF3 activation, resu

30 are being developed to augment and optimize STING activation as a cancer therapy.

31 infection of macrophages, RECON antagonized STING activation by acting as a molecular sink for cdNs.

32 ocytes, which is distinct from the effect of STING activation by DMXAA on enhancing proinflammatory r

33 r knowledge we provide the first evidence of STING activation in T cells, in which STING agonists not

34 I interferons (IFNs) is the major outcome of STING activation in vertebrates, it has recently become

35 We propose that radiation-induced STING activation is immunosuppressive due to (monocytic)

36 In this study, we show that STING activation reduces the proliferation of T lymphocy

37 nct from the antiviral state associated with STING activation.

38 ium, we postulated that AMPK participates in STING activation; however, its role has yet to be been d

39 Here, we show that IDO activity induced by STING activity in the tumor microenvironment (TME) promo

40 These data provide evidence that the NTD of STING affects DNA responses via control of trafficking.

41 howed enhanced generation of cyclic GMP-AMP, STING aggregation, and TANK-binding kinase 1 and IFN reg

42 ronic lymphocytic leukemia, injection of the STING agonist 3'3'-cGAMP induced apoptosis and tumor reg

43 valuated the adjuvant activity of the potent STING agonist, CDN 3'3'-cGAMP (cGAMP), encapsulated in a

44 Our results suggest a re-evaluation of STING agonist-based therapies may be necessary to identi

45 We assessed a panel of TLR and STING agonists (a) for their ability to reprogram macrop

46 As a result, STING agonists administered in a soluble form have elici

47 pathway, enhancing the anti-tumor effects of STING agonists and radiotherapy.

48 ce for potentially developing cGAMP or other STING agonists as a new class of immune-stimulating long

49 ility to boost antitumoral immune responses, STING agonists can also directly eradicate malignant B c

50 mmunosuppressive effects of radiotherapy and STING agonists can be abrogated in humans by a translati

51 ng immunogenic tumor growth and accordingly, STING agonists induce regression of therapy-resistant tu

52 nce of STING activation in T cells, in which STING agonists not only provoke type I IFN production an

53 tical mediator of type I IFN production, and STING agonists such as cGMP-AMP (cGAMP) and other cyclic

54 Delivery of STING agonists via particle platforms has proven a more

55 that codelivery of stimulator of IFN genes (STING) agonists stimulates immune responses to eliminate

56 ion similar to what we observe with the MOLF Sting allele, a crucial functional difference not appare

57 to desensitize people suffering from insect sting allergies.

58 Although STING also induced IDO in tumor-draining lymph nodes (TD

59 Stimulator of interferon genes (STING, also known as MITA, MPYS, or ERIS) is an exciting

60 First-line treatment for Hymenoptera sting anaphylaxis is intramuscular adrenaline.

61 antigen (eg, certain foods or single insect stings), anaphylaxis can be considered the most aberrant

62 Additionally, we determined that STING and cyclic GMP-AMP synthase (cGAS) are important t

63 Indeed, we found that both proteins STING and IFI16 were eliminated in cells constitutively

64 TMEM173 encodes MPYS/STING and is an innate immune sensor for cyclic dinucleo

65 lammatory gene activation via its effects on STING and NF-kappaB.

66 by STING stimuli, through the elimination of STING and of interferon-inducible protein 16 (IFI16); (i

67 d ISG expression; and (v) UL46 binds to both STING and TBK1 through different domains.

68 trated that UL46 via its N terminus binds to STING and, via its C terminus, to TBK1.

69 14-year-old boy had no history of jellyfish stings and had been eating commercially available jellyf

70 c acids by cytosolic receptors, dependent on STING, and endosomal sensors, dependent on Unc93b1, can

71 required for the cGAMP-induced activation of STING, and interacts with STING to promote STING phospho

72 P synthase (cGAS), the innate immune adaptor STING, and interferon signaling.

73 osolic surveillance pathway involving DDX41, STING, and other downstream molecular targets of L. mono

74 matory cytokine secretion by monocytes, in a STING- and inflammasome-dependent manner.

75 dsDNA itself was sufficient to induce cGAS-, STING-, and interferon signaling-dependent ISG15 monomer

76 zed by viral proteins to inhibit cGAS and/or STING are also discussed.

77 Autosomal dominant mutations in STING are thought to trigger activation of IRF3 and subs

78 The identification of STING as a key cytoplasmic innate recognition molecule f

79 atients with stimulator of interferon genes (STING)-associated vasculopathy with onset in infancy (SA

80 y manifestations also exist in patients with STING-associated vasculopathy in infancy (SAVI).

81 tions such as Aicardi-Goutieres syndrome and STING-associated vasculopathy of infancy (SAVI).

82 tly described type I interferonopathy called STING-associated vasculopathy with onset in infancy (SAV

83 Here we show that palmitoylation of STING at the Golgi is essential for activation of STING.

84 tead, detection of cytosolic DNA by the cGAS-STING axis induces a cell death program initiating potas

85 cytosolic DNA recognition, in which the cGAS-STING axis triggers antiviral immunity, whereas AIM2 tri

86 echanism that dampens activation of the cGAS-STING axis.

87 Furthermore, we determined that STING but not cGAS is critical for host protection again

88 the pattern recognition receptor and adaptor STING but not cGAS.

89 dependent on stimulator of interferon genes (STING), but not the Toll-like receptor or the mitochondr

90 Disruption of STING, but not cGAS or IRF3, attenuated cell death, sugg

91 cells, implying that prolonged activation of STING can lead to apoptosis.

92 tional significance of polymorphisms in MOLF STING can provide basic mechanistic insights relevant to

93 Hymenoptera stings can cause severe anaphylaxis in untreated venom-a

94 Whereas in free-living cnidarians the stinging capsules are used for prey capture or defense,

95 wn as polar capsules, akin to the nematocyst stinging capsules of free-living species.

96 cognition by stimulator of interferon genes (STING)-cGAS impaired interferon signalling.

97 trate that a cationic polymer can engage the STING-cGAS pathway to trigger innate and adaptive immune

98 ients who had undergone controlled honey bee sting challenge after at least 6 months of HBV immunothe

99 presence of systemic allergic reactions upon sting challenge.

100 ely after allergic sting reactions or before sting challenges and 4 weeks later.

101 All sting challenges were tolerated.

102 E and sIgG4 remained completely stable after sting challenges.

103 t and activation of TANK-binding kinase 1 in STING complex.

104 Several human alleles of STING confer attenuated IFN-I production similar to what

105 IF in STING signaling: various activators of STING could not induce genes in the absence of TRIF.

106 e innate immunity cytosolic DNA-sensing cGAS-STING (cyclic GMP-AMP synthase linked to stimulator of i

107 HIV-1 evades immune detection by the cGAS-STING cytosolic DNA-sensing pathway during acute infecti

108 PGL activated the STING cytosolic sensing pathway in resident macrophages,

109 ith DNA viruses, resulting in degradation of STING, decreased interferon signaling and increased path

110 ory and metabolic phenotypes by showing that Sting deficiency rescued both inflammatory and metabolic

111 lication is strongly increased in neurons in STING-deficient mice.

112 , TRIF-related adaptor molecule (TRAM)-, and STING-deficient mice.

113 pathway and stimulator of interferon genes (STING)-dependent cytokine secretion.

114 Interestingly, HSV-infected microglia confer STING-dependent antiviral activities in neurons and prim

115 fusion stimulates interferon production in a STING-dependent but cGAS-independent manner.

116 Thus, our results show how STING-dependent DNA sensing can enhance tolerogenic stat

117 t mitochondrial membrane potential regulates STING-dependent IFN-beta induction independently of ATP

118 ve accrual of undegraded DNA leads to both a STING-dependent inflammatory arthritis and additional Un

119 , some of these cAIMP analogs induce greater STING-dependent IRF and NF-kappaB pathway signaling than

120 pha induction following stimulation with the STING-dependent ligand 5,6-dimethyl xanthnone-4-acetic a

121 754) is directly phosphorylated by TBK1 in a STING-dependent manner.

122 duced macrophage type I IFN expression via a STING-dependent pathway and promoted S. aureus intracell

123 a production almost exclusively through cGAS-STING-dependent recognition of bacterial DNA.

124 y as a cell-autonomous response mobilized by STING-dependent sensing of a specific vita-PAMP and eluc

125 cumulative effect of DNA sensing by cGAS and STING-dependent sensing of c-di-AMP.

126 ally to DMXAA, indicating that AMPK promotes STING-dependent signaling independent of ULK1 in mouse c

127 conclusion, these findings suggest that the STING-dependent type I IFN pathway is critical for the G

128 eltaICP0 virus infection have defects in the STING DNA-sensing pathway, which partially accounts for

129 onclude that UL46 counteracts the actions of STING during HSV-1 infection.

130 ractions appear to modulate the functions of STING during HSV-1 infection.

131 a/beta signaling or stimulator of IFN genes (STING) exhibit exacerbated neurovirulence and atypical l

132 Disruption of STING expression in endothelial cells by clustered regul

133 Restoration of STING expression in these cells rescued innate immunity

134 Restoration of STING expression resulted in suppression of DeltaICP0 vi

135 Importantly, introduction of STING expression specifically in hepatocytes reconstitut

136 Similarly, STING failed to promote growth of B16 melanoma or to ind

137 developed a systemic allergic reaction after sting from an unknown creature while diving.

138 NLRX1 sequesters the DNA-sensing adaptor STING from interaction with TANK-binding kinase 1 (TBK1)

139 nt reported prior episodes of swelling after stings from several different creatures, including jelly

140 target in innate immune cells; more recently STING has also been shown to detect endogenous DNA and p

141 Thus far STING has been studied in macrophages and dendritic cell

142 to develop novel antidotes against scorpion stings has achieved excellent results.

143 host protein Stimulator of Interferon Genes (STING) has been shown to be essential for recognition of

144 Recently, cGAS and STING have been identified as intracellular sensors that

145 ic GAMP (2'3'-cGAMP), the natural agonist of STING (i.e., stimulator of interferon genes) or after in

146 ein UL46 interacts with and colocalizes with STING; (ii) UL46 expressed out of the context of the inf

147 -intrinsic dsDNA sensing dependent upon cGAS-STING.IMPORTANCE By antagonizing type I interferon produ

148 or and kinase S6K1 and the signaling adaptor STING in a manner dependent on the DNA sensor cGAS.

149 However, the role of STING in adaptive immunity is still unknown.

150 This study underscores the importance of STING in the control of HSV-1.

151 Ablation of STING in the G37S mice results in partial rescue of the

152 identify that IRF3, by its association with STING in the presence of ER stress, couples hepatocyte a

153 We supposed that stings in skin areas, which are well supplied with blood

154 STING incites spontaneous immunity during immunogenic tu

155 ponse genes, via an atypical IRF1-dependent, STING-independent mechanism.

156 Endogenous STING inhibited proliferation of mouse T lymphocytes.

157 us-host stand-off in the context of the cGAS-STING innate immune pathway.

158 ironmental factors, including aeroallergens, stinging insects, fungi, pollutants, viral respiratory t

159 function, of S6K1 was required for the S6K1-STING interaction and that the TBK1 critically promoted

160 ociates with NLRC3 and can disrupt the NLRC3-STING interaction in the cytosol of human epithelial cel

161 cyclic GMP-AMP synthase (cGAS), its adaptor STING, IRF3, or the type I IFN receptor IFNAR exhibited

162 f components of the STING pathway, including STING, IRF3, Tbk1, extracellular IFNbeta, and the Jak-St

163 Our work therefore links the STING-IRF3 axis to enhanced IL-12 production and intrace

164 The cGAS-cGAMP-STING-IRF3 pathway of cytosolic DNA sensing plays a pivo

165 STING is a critical mediator of type I IFN production, a

166 f DNA in the cytoplasm activates cGAS, while STING is activated by cyclic dinucleotides (cdNs) produc

167 Consistently, in mice, STING is necessary for the first phase of IFN-I producti

168 Although STING is redundant for cell-autonomous antiviral resista

169 t to engage the type I IFN pathway, but only STING is required to induce IL-1beta secretion, caspase-

170 The stimulator of interferon (IFN) genes (STING) is a broad antimicrobial factor that restricts he

171 sensor stimulator of interferon (IFN) genes (STING) is critical for IFN and inflammatory gene express

172 Stimulator of interferon genes (STING) is essential for the type I interferon response a

173 oints included additional VAS items (burning/stinging, itching, foreign body sensation, eye discomfor

174 mmunity, but both effects were alleviated in STING knockdown cells.

175 played growth defects, which were rescued in STING knockdown cells; (iv) the DeltaUL46 virus failed t

176 inding proteins (GBPs), are downregulated in STING knockout (KO) macrophages infected with Brucella o

177 We conclude that targeting the cGAS-STING-LCD-NLRP3 pathway will ameliorate pathology in inf

178 ha after treatment with DMXAA or the natural STING ligand cyclic GMP-AMP (cGAMP).

179 that the inflammatory pathways activated by STING ligands generate a powerful adjuvant activity for

180 Moreover, STING loss prevented the regression of abscopal tumours

181 show that the pLxIS motif of phosphorylated STING, MAVS, and TRIF binds to IRF-3 in a similar manner

182 possibility that the ancestral functions of STING may have included activation of antibacterial immu

183 Toll-like receptors (TLRs), is essential for STING-mediated innate antiviral immunity as well as pro-

184 n of self-DNA in the cytoplasm, triggering a STING-mediated innate immune response after replication

185 evidence of a cGAS-independent mechanism of STING-mediated protection against an intracellular bacte

186 IRF3, attenuated cell death, suggesting that STING mediates Chlamydia-induced cell death independent

187 nfected as larvae also had a more queen-like sting morphology.

188 observed only mild up-regulation of ISGs in STING N153S fibroblasts and splenocytes and STING N154S

189 We generated heterozygous STING N153S knock-in mice as a model of SAVI.

190 STING N153S mice lacking IRF3 also developed lung diseas

191 of-flight (CyTOF) analysis revealed that the STING N153S mutation caused myeloid cell expansion, T ce

192 Thus, the SAVI-associated STING N153S mutation triggers IRF3-independent immune ce

193 STING N153S fibroblasts and splenocytes and STING N154S SAVI patient fibroblasts.

194 Importantly, the cGAS-STING-NLRP3 pathway constitutes the default inflammasome

195 ticle, we identify novel mutations in NTD of Sting of the MOLF strain in response to HSV and Listeria

196 Conversely, the effects of STING on T cells could potentially be harnessed for ther

197 frequently by epigenetic silencing of either STING or the cyclic GMP-AMP synthase, which generates ST

198 By contrast, the absence of TLR2, STING, or the addition of TLR4 agonist has no effect.

199 Unilateral face, neck and ear pain, stinging pain, foreign body sensation and dysphagia can

200 mune response, pharmacologic agonists of the STING pathway are being developed to augment and optimiz

201 xpected new activity of GCV and identify the STING pathway as a regulator of microglial reactivity an

202 ecome clear that core components of the cGAS-STING pathway evolved more than 600 million years ago, p

203 genomic DNA and reveal the role of the cGAS/STING pathway in the induction of type I IFN in response

204 The role of STING pathway in the selectivity of HSV has been address

205 However, their relation to the cGAS-STING pathway is not clear.

206 inucleotide 2',3'-cGAMP, suggesting that the STING pathway may be compromised.

207 re, we show that IFI16 functions in the cGAS-STING pathway on two distinct levels.

208 ion in the CNS by microglia through the cGAS-STING pathway orchestrates an antiviral program that inc

209 ection of cyclic dinucleotides (cdNs) by the STING pathway potently triggers the antiviral response.

210 The cytoplasmic chromatin-cGAS-STING pathway promotes the senescence-associated secreto

211 ng kinase), independent from the alternative STING pathway triggered by membrane fusion of enveloped

212 discuss the evolutionary origins of the cGAS-STING pathway, and consider the possibility that the anc

213 mmunosuppression following activation of the STING pathway, enhancing the anti-tumor effects of STING

214 recent advances in understanding of the cGAS-STING pathway, focusing on the regulatory mechanisms and

215 Inhibition of components of the STING pathway, including STING, IRF3, Tbk1, extracellula

216 stimulated genes that may be induced by the STING pathway, these results have broad implications in

217 ed, Irf7-dependent signaling, as part of the Sting pathway, was critical for generation of both innat

218 ped RNA viruses stimulate a cGAS-independent STING pathway, which is targeted by IAV.

219 ke receptors and the recently described cGAS-STING pathway.

220 eltaICP0 HSV-1 is in part due to an impaired STING pathway.IMPORTANCE The DNA sensor STING plays pivo

221 Attenuating Sting, phosphorylated Tbk1 and, importantly, blocking re

222 n of the IFN-beta signaling molecules DDX41, STING, phosphorylated TBK1, and phosphorylated p38 MAPK

223 f STING, and interacts with STING to promote STING phosphorylation and translocation.

224 s innate and adaptive immunity in which host STING plays an important role.

225 ired STING pathway.IMPORTANCE The DNA sensor STING plays pivotal role in controlling HSV-1 infection

226 n these cells by transient expression of the STING protein but not after overexpression of interferon

227 ations at positions 206, 281, and 284 of the STING protein define a novel cluster of amino acids with

228 at positions 206, 281, and 284 of the human STING protein.

229 depending on the severity of their previous sting reaction(s).

230 r adverse events and for relapse of systemic sting reaction, and a summary of gaps in the evidence.

231 educe the risk of subsequent severe systemic sting reactions (OR = 0.08, 95% CI 0.03-0.26); meta-anal

232 ctive in reducing severe subsequent systemic sting reactions and in improving disease-specific qualit

233 e in those at high risk of repeated systemic sting reactions and/or impaired quality of life.

234 Systemic-allergic sting reactions have been reported in up to 7.5% of adul

235 e only treatment to prevent further systemic sting reactions is venom immunotherapy.

236 v 5 were measured immediately after allergic sting reactions or before sting challenges and 4 weeks l

237 ts, 85 allergic patients with acute systemic sting reactions, and 61 allergic patients currently trea

238 prevent further moderate-to-severe systemic sting reactions.

239 lar microbial nucleic acid sensors, TLR3 and STING, recognize pathogen molecules and signal to activa

240 STING recruits TNFR-associated NF-kappaB kinase-binding

241 to dephosphorylation at Ser-555 of the known STING regulator, UNC-51-like kinase 1 (ULK1).

242 Inhibition of cell proliferation by STING required its relocalization to the Golgi apparatus

243 fection of hepatocytes, which do not express STING, revealed that RECON negatively regulates NF-kappa

244 hem sensory pathway components such as cGAS, STING, RIG-I, MDA5, and the transcription factor IRF7, w

245 iral immunity; however, a major hindrance is STING's cytosolic localization which requires intracellu

246 Mice deficient in STING show impaired immuno-surveillance of oncogenic RAS

247 itutive active mutations in TMEM173 encoding STING showed impaired proliferation and reduced numbers

248 Four weeks after the sting, sIgE and sIgG4 levels were increased in allergic

249 s reveal a greater complexity in the role of STING signaling in cancer, underscoring how innate immun

250 Extrinsic STING signaling is also needed for antigen-presenting ce

251 Here, we show that STING signaling is recurrently suppressed in melanoma ce

252 Our results indicate that defective STING signaling may be responsible for the observed gene

253 In contrast with native LLC tumors, STING signaling neither promoted growth of neoantigen-ex

254 rpes simplex virus (HSV), which triggers the STING signaling pathway and is controlled by it, replica

255 diate cytosolic immune responses through the STING signaling pathway, although evidence suggests that

256 robial pathogens depends on a conserved cGAS-STING signaling pathway.

257 Mechanistically, STING signaling was suppressed most frequently by epigen

258 ere, we report an essential role for TRIF in STING signaling: various activators of STING could not i

259 27-dependent targeting of the TBK1-activated STING signalsome.

260 The innate immunoregulator STING stimulates cytokine production in response to the

261 The adaptor proteins STING (stimulator of IFN genes), MAVS (mitochondrial ant

262 ection blocks type I interferon triggered by STING stimuli, through the elimination of STING and of i

263 lock innate immunity triggered by ligands of STING such as 2',3'-cGAMP and also activated IFN-beta an

264 -GMP is known to stimulate the innate sensor STING, surprisingly, the DeltabpdA mutant induced a weak

265 We hope to exploit our findings to develop STING-targeted immunotherapies.

266 The formation of a tripartite S6K1-STING-TBK1 complex was necessary for the activation of I

267 lates type I IFN expression through the cGAS-STING-TBK1 signaling axis.

268 kinase-interferon regulatory factor 3 (cGAS-STING-TBK1-IRF3) signaling pathway.

269 erferon response that required the host cGAS/STING/TBK1/IRF3 signaling pathway.

270 but required a distinct C-terminal domain of STING that activates NF-kappaB.

271 ar stomatitis virus (VSV), a virus sensed by STING that can cause an influenza-like illness in humans

272 Further, IAV interacts with STING through its conserved hemagglutinin fusion peptide

273 ar redistribution and effective signaling of STING, thus blunting the transcription of type I IFNs.

274 P-1 pathway are required for the function of STING (TMEM173), an ER-resident transmembrane protein cr

275 nterferon response by localizing ER-resident STING to autophagosomes.

276 that binds and activates the adaptor protein STING to induce type I interferons (IFNs) and other immu

277 s cyclic GMP-AMP (cGAMP) binds and activates STING to induce type I interferons.

278 innate signaling in a manner independent of STING to promote an antibacterial state.

279 uced activation of STING, and interacts with STING to promote STING phosphorylation and translocation

280 urn binds to stimulator of interferon genes (STING) to activate IFN-I.

281 DNA engages stimulator of interferon genes (STING) to activate TANK-binding kinase 1 (TBK1), which s

282 nnate sensor stimulator of interferon genes (STING) to mediate endoplasmic reticulum (ER) stress.

283 d subsequent studies revealed that activated STING traffics to the lysosome, where it triggers membra

284 presence of DNA and/or cyclic dinucleotides, STING translocates from the endoplasmic reticulum to per

285 nd the stimulator of interferon (IFN) genes (STING), two crucial host factors involved in DNA detecti

286 The STING/type I interferon pathway enhances suppressive inf

287 73) encoding stimulator of interferon genes (STING) underlie a recently described type I interferonop

288 STING variants that constitutively induce the type I int

289 Immunological responses after stings varied in bee and vespid venom-allergic patients.

290 Upon stimulation, STING was degraded less efficiently in B cells, implying

291 Clinically, STING was found to be expressed extensively in human pan

292 Importantly, functional STING was necessary for GCV to inhibit inflammation in c

293 Consistently, STING was necessary to mount the first phase of IFN-I pr

294 acid (PGA) which is a component of jellyfish stings was negative.

295 Stimulator of interferon genes (STING) was initially described as a sensor of intracellu

296 omics [7, 12] to resolve relationships among stinging-wasp families, gathering sequence data from >80

297 ea are identified as the sister group of the stinging wasps (Aculeata).

298 The stinging wasps (Hymenoptera: Aculeata) are an extremely

299 present a highly supported phylogeny of the stinging wasps.

300 ng morphotypes unknown in solitary aculeate (stinging) wasps, providing insight into early behavior.