ライフサイエンスコーパス: DGC

1 DGC activity of GcbA was required for its function, as a

2 DGC deficiency in humans results in muscular dystrophy,

3 DGCs generated neonatally were compared with those gener

4 DGCs have long been implicated in TLE, because they regu

5 DGCs were also labeled after injections into the anterio

6 with 3 or more cases of DGC; families with 1 DGC before the age of 40; and families with a history of

7 with a reduced number of activated egr-1(+) DGCs in Tau(VLW) mice.

8 is represents the first description of (1) a DGC post-transcriptionally activated by direct pairing w

9 tation of the alpha-sarcoglycan gene, also a DGC component, causes LGMD2D and represents the most com

10 xpressing newborn cells began to establish a DGC-like morphology at approximately 7 d after birth, wi

11 mple spindle-like morphology develops into a DGC, consisting of a single apical dendrite with further

12 ow that the inner membrane protein NicD is a DGC that controls dispersal by sensing nutrient levels:

13 inantly a PDE, while CdgB is predominantly a DGC.

14 o Alg44 (a PilZ protein) or regulate WspR (a DGC enzyme that has been shown to bind to dimeric c-di-G

15 nce that aberrant integration of post-SE, AB DGCs contributes to increased synaptic drive and support

16 ulnerability to SE, indicating that abnormal DGC plasticity derives exclusively from aberrantly devel

17 If abnormal DGCs do contribute, a reasonable prediction would be tha

18 or decades, direct evidence linking abnormal DGCs to seizures has been lacking.

19 While the presence of abnormal DGCs in epilepsy has been known for decades, direct evid

20 Here, we isolate the effects of abnormal DGCs using a transgenic mouse model to selectively delet

21 rrelated with the number or load of abnormal DGCs.

22 tion of the mTOR pathway, producing abnormal DGCs morphologically similar to those in epilepsy.

23 e in support of the hypothesis that abnormal DGCs contribute to the development of TLE and also suppo

24 s in about 4 weeks, confirming that abnormal DGCs, which are present in both animals and humans with

25 ulation-rather than the previously activated DGC ensembles that responded to past events-was selected

26 oreover, ECA3270 represents the first active DGC reported to have an alternative active-site motif fr

27 l neurons by increasing the firing of active DGCs.SIGNIFICANCE STATEMENT Adult brains are constantly

28 For the first time, we found that active DGCs responded to a novel experience by increasing their

29 ike OdaA, which did not significantly affect DGC activity of SadC, OdaI inhibited c-di-GMP production

30 DGCs) fail to develop - including nearly all DGCs in the dorsal hippocampus - secondary to eliminatin

31 doscopy and clinicopathology between PGC and DGC.

32 M injections both retinal ganglion cells and DGCs were labeled.

33 rentially affects LapA localization, another DGC mainly controls swimming motility, while a third DGC

34 To examine the relationship between DGC birthdate, morphology, and network integration in a

35 ntration was significantly different between DGCs, suggesting that bacteria can optimize phenotypic o

36 esult of a sophisticated interaction between DGCs and PDEs.

37 higher DGC activity of the diferrous Vc Bhr-DGC is consistent with induction of biofilm formation in

38 Vc Bhr-DGC showed approximately 10 times higher DGC activity in

39 This protein, Vc Bhr-DGC, was found to contain two tightly bound non-heme iro

40 tory and inhibitory currents from birthdated DGCs.

41 born DGCs transiently reorganized adult-born DGC local afferent connectivity and promoted global rema

42 DGCs preferentially synapse onto adult-born DGCs after pilocarpine-induced status epilepticus (SE),

43 ture DGCs enhanced integration of adult-born DGCs and increased NSC activation.

44 statin(-) interneuron inputs onto adult-born DGCs are maintained, likely due to preferential sproutin

45 Adult-born DGCs are thought to compete with mature DGCs for inputs

46 jections that specifically target adult-born DGCs arise in the epileptic brain, whereas axons of inte

47 he DG by enhancing integration of adult-born DGCs in adulthood, middle age, and aging enhanced memory

48 Enhanced integration of adult-born DGCs transiently reorganized adult-born DGC local affere

49 onveyed to RGLs, progenitors, and adult-born DGCs via the neurogenic niche that is composed of divers

50 mature DGCs increased survival of adult-born DGCs without affecting proliferation or DGC activity.

51 The events leading adult-born DGCs' to transition from simple spindle-like morphology

52 SC) homeostasis and maturation of adult-born DGCs.

53 d, expanded cohort of age-matched adult-born DGCs.

54 lating the initial integration of adult-born DGCs.SIGNIFICANCE STATEMENT Since the discovery of the c

55 nputs are greatly diminished onto early-born DGCs after SE.

56 Both adult-born and early-born DGCs are targets of new inputs from other DGCs as well a

57 naptic inputs onto adult-born and early-born DGCs in the rat pilocarpine model of mTLE.

58 er their integration differs from early-born DGCs that are mature at the time of epileptogenesis.

59 re to preferentially synapse onto early-born DGCs.

60 synapse onto both adult-born and early-born DGCs.

61 particularly on those proteins bearing both DGC and PDE modules, and for future optimization studies

62 Further studies show that both DGCs are essential for the Hfq-mediated post-transcripti

63 ow-specificity signaling is characterized by DGCs or PDEs that modulate a general signal pool, which,

64 ciated with risk for diffuse gastric cancer (DGC) and lobular breast cancer.

65 tient diagnosed with diffuse gastric cancer (DGC) before age 50; families with 3 or more cases of DGC

66 (PGC, n = 131) and distal gastric carcinoma (DGC, n = 307) in consecutive 438 EGCs diagnosed with the

67 A1 neuron populations, dentate granule cell (DGC) ensembles activated by learning were not preferenti

68 ICANCE STATEMENT Adult dentate granule cell (DGC) neurogenesis is altered in rodent models of tempora

69 Dentate granule cell (DGC) neurogenesis persists throughout life in the hippoc

70 h a major focus on the dentate granule cell (DGC) population, to explore the signaling pathways under

71 unctions of adult-born dentate granule cell (DGCs) are poorly understood.

72 retinal input from displaced ganglion cells (DGCs), which are found at the margin of the inner nuclea

73 pocampus give rise to dentate granule cells (DGCs) and astrocytes throughout life, a process referred

74 nputs onto adult-born dentate granule cells (DGCs) are altered in experimental mesial temporal lobe e

75 when adult-generated dentate granule cells (DGCs) are approximately 4 weeks of age, a time point whe

76 Newborn dentate granule cells (DGCs) are continuously generated in the adult brain.

77 New dentate granule cells (DGCs) are continuously generated, and integrate into the

78 Newborn dentate granule cells (DGCs) are generated in the hippocampal dentate gyrus (DG

79 pyramidal neurons and dentate granule cells (DGCs) by voltage clamp technique.

80 the vast majority of dentate granule cells (DGCs) fail to develop - including nearly all DGCs in the

81 leptogenesis, adult-generated granule cells (DGCs) form aberrant neuronal connections with neighborin

82 Most dentate granule cells (DGCs) generated in response to an epileptic insult devel

83 Dentate granule cells (DGCs) have a single, complex, apical dendrite.

84 d newborn hippocampal dentate granule cells (DGCs) in acute mouse brain slices, we found that DA not

85 s of adult-born mouse dentate granule cells (DGCs) in vivo and found that they underwent over-branchi

86 ult-born, hippocampal dentate granule cells (DGCs) is hypothesized to contribute to the development o

87 s by which adult-born dentate granule cells (DGCs) modulate pattern separation to influence resolutio

88 ogical alterations in dentate granule cells (DGCs) of FTD patients and in a mouse model of the diseas

89 nts generates newborn dentate granule cells (DGCs) throughout life.

90 rgic action occurs in dentate granule cells (DGCs), located at the first stage of the hippocampal tri

91 FGF22 on the axons of dentate granule cells (DGCs), which are presynaptic to CA3 pyramidal neurons, i

92 nuous addition of new dentate granule cells (DGCs), which is regulated exquisitely by brain activity,

93 ipal cells of the DG, dentate granule cells (DGCs).

94 Human mutations in the dystroglycan complex (DGC) result in not only muscular dystrophy but also cogn

95 mbly of the dystrophin-glycoprotein complex (DGC) are associated with a spectrum of brain abnormaliti

96 loss of the dystrophin glycoprotein complex (DGC) from the sarcolemma which contributes to the dystro

97 The dystrophin-glycoprotein complex (DGC) links the muscle cytoskeleton to the extracellular

98 The dystrophin-glycoprotein complex (DGC) provides an essential link from the muscle fibre cy

99 The dystrophin-glycoprotein complex (DGC), a multicomponent transmembrane complex linking the

100 mbly of the dystrophin-glycoprotein complex (DGC), and a defective DGC disrupts an essential link bet

101 sembles the dystrophin-glycoprotein complex (DGC), but lacks actin-binding domains.

102 rix via the dystrophin-glycoprotein complex (DGC), exhibit muscular dystrophy, cardiomyopathy, and im

103 through the dystrophin-glycoprotein complex (DGC).

104 eins of the dystrophin-glycoprotein complex (DGC).

105 dystrophin-associated glycoprotein complex (DGC).

106 tion of the dystrophin-glycoprotein complex (DGC).

107 nent of the dystrophin-glycoprotein complex (DGC).

108 - and utrophin (Utr)-glycoprotein complexes (DGC and UGC).

109 nner membrane-localized diguanylate cyclase (DGC) and a known regulator of cellulose biosynthesis.

110 codes two proteins with diguanylate cyclase (DGC) and phosphodiesterase (PDE) domains that modulate t

111 a often encode multiple diguanylate cyclase (DGC) and phosphodiesterase (PDE) enzymes that produce an

112 enes encoding predicted diguanylate cyclase (DGC) and phosphodiesterase proteins (ECA3270 and ECA3271

113 i-GMP is synthesized by diguanylate cyclase (DGC) enzymes and hydrolyzed by phosphodiesterase (PDE) e

114 s inversely governed by diguanylate cyclase (DGC) enzymes and phosphodiesterase (PDE) enzymes, which

115 ovide evidence that the diguanylate cyclase (DGC) GcbA contributes to the regulation of BdlA cleavage

116 ecifically requires the diguanylate cyclase (DGC) SadC, and epistasis analysis indicates that PilY1 f

117 tonic PAO1 requires the diguanylate cyclase (DGC) SadC, previously identified as a regulator of surfa

118 lation of the mRNA of a diguanylate cyclase (DGC), Vca0939; relieving an inhibitory structure in vca0

119 itory site (I-site) of diguanylate cyclases (DGCs) and compared it to the conformation adopted in the

120 P metabolism proteins, diguanylate cyclases (DGCs) and phosophodiesterases (PDEs), usually lead to di

121 Opposing activities of diguanylate cyclases (DGCs) and phosphodiesterases (PDEs) control c-di-GMP hom

122 e development-specific diguanylate cyclases (DGCs) CdgB and CdgC, and the c-di-GMP phosphodiesterases

123 di-GMP is catalyzed by diguanylate cyclases (DGCs) containing the GGDEF domain, while its degradation

124 and contains numerous diguanylate cyclases (DGCs) for synthesizing c-di-GMP and phosphodiesterases (

125 Two diguanylate cyclases (DGCs) HmsT and Y3730 (HmsD) are responsible for biofilm

126 n annotation regarding diguanylate cyclases (DGCs) in this bacterium.

127 re predicted to encode diguanylate cyclases (DGCs) or phosphodiesterases (PDEs) were screened for the

128 rmation, with multiple diguanylate cyclases (DGCs) playing distinct roles in these processes, yet lit

129 cteristic of bacterial diguanylate cyclases (DGCs) that catalyze formation of cyclic di-(3',5')-guano

130 -GMP is synthesized by diguanylate cyclases (DGCs) that contain a GGDEF domain and is degraded by pho

131 clic di-GMP (c-di-GMP) diguanylate cyclases (DGCs), GcpA and GcpL, are repressed by Hfq.

132 -GMP is synthesized by diguanylate cyclases (DGCs).

133 e and discovered that loss of SSPN decreased DGC and UGC abundance, leading to impaired laminin-bindi

134 -glycoprotein complex (DGC), and a defective DGC disrupts an essential link between the intracellular

135 nscription factors, PilZ domains, degenerate DGCs or PDEs, and riboswitches.

136 Qrr-dependent DGC activation led to c-di-GMP accumulation and biofilm

137 rives exclusively from aberrantly developing DGCs.

138 These findings indicate that developing DGCs exhibit maturation-dependent vulnerability to SE, i

139 Bacteria typically encode many different DGCs and PDEs within their genomes.

140 Therefore, selecting distinct DGC populations to represent similar but not identical i

141 s can be specifically controlled by distinct DGCs.

142 In a dual DGC and PDE-A reaction, excess pGpG extends the half-lif

143 ioselective four-dimensional dynamic GC (e4D-DGC) approach to study reversible molecular interconvers

144 Our results demonstrate that hilar ectopic DGCs preferentially synapse onto adult-born DGCs after p

145 ency and (1) the percentage of hilar ectopic DGCs, (2) the amount of mossy fiber sprouting, and (3) t

146 e or after SE decreased MFS or hilar ectopic DGCs, supporting the RV labeling results.

147 ptic drive and support the idea that ectopic DGCs serve as putative hub cells to promote seizures.SIG

148 crobes have a large number of genes encoding DGCs and PDEs that are predicted to be part of c-di-GMP

149 Finally, optogenetic silencing of existing DGCs during novel environmental exploration perturbed ex

150 manipulation, we revealed that pre-existing DGCs actively regulated microvascular blood flow.

151 P. aeruginosa homolog of the P. fluorescens DGC GcbA involved in promoting biofilm formation via reg

152 hat are PLP had histopathologic evidence for DGC on endoscopy and/or gastrectomy.

153 These experiments support a role for DGCs in enhancing spatial learning and memory.

154 lm formation and illustrate a novel role for DGCs in the regulation of the reverse sessile-motile tra

155 raction analysis revealed that at least four DGCs, together with CdgJ, control motility in V. cholera

156 es were observed in recordings obtained from DGCs from refractory SE animals.

157 ly suggests that YeaJ is indeed a functional DGC.

158 out the potential conservation of functional DGCs across Pseudomonas species.

159 Furthermore, DGCs are unusual in that they are continually generated

160 and integration, but whether adult-generated DGCs contribute to the development of epilepsy is contro

161 d (but not 6- or 8-week-old) adult-generated DGCs strongly activated CA3 interneurons.

162 f 4-week-old (but not older) adult-generated DGCs.

163 enic mouse model to fate map adult-generated DGCs.

164 ively delete PTEN from postnatally generated DGCs.

165 dition, expression of CdgB or a heterologous DGC in strain KKF457 stimulated F. novicida biofilms, ev

166 The higher DGC activity of the diferrous Vc Bhr-DGC is consistent w

167 Bhr-DGC showed approximately 10 times higher DGC activity in the diferrous than in the diferric form.

168 eriplasmic domain Y3729 (HmsC) inhibits HmsD DGC activity in vitro while an outer membrane Pal-like p

169 strophic or very old animals, disruptions in DGC structure and function impair lateral transmission o

170 neurons also show a significant reduction in DGC and GABA receptor distribution as well as abnormal n

171 cantly more frequent (32.1%, versus 12.1% in DGCs), as were mucinous and neuroendocrine carcinomas, c

172 nvaded deeper (22.9% into SM2, versus 13% in DGCs), but had fewer (2.9%, versus 16.7% in DGCs) lymph

173 showed shorter (42.4 months, versus 48.3 in DGCs) survival.

174 ly different from those (32.6% and 64.5%) in DGCs.

175 a with lymphoid stroma (6.9%, versus 1.6% in DGCs); but poorly cohesive carcinoma was significantly l

176 DGCs), but had fewer (2.9%, versus 16.7% in DGCs) lymph node metastases.

177 icantly less frequent (5.3%, versus 35.8% in DGCs).

178 smaller (1.9 cm in average, versus 2.2 cm in DGCs), invaded deeper (22.9% into SM2, versus 13% in DGC

179 tion of distinct subtypes of DA receptors in DGCs at different developmental stages.

180 and promote a similar dendrite structure in DGCs.

181 ity signaling is characterized by individual DGCs or PDEs that are specifically associated with downs

182 e decision to fire or not fire by individual DGCs was robust and repeatable at all stages of developm

183 However, individual DGCs showed a significant correlation between c-di-GMP p

184 o track the real-time activity of individual DGCs in freely behaving mice.

185 ically upregulated for ectopically localized DGCs.

186 We found that AB, ectopically located DGCs exhibit the most pro-excitatory physiological chang

187 veloping during SE revealed normally located DGCs exhibiting hilar basal dendrites and mossy fiber sp

188 RV injections 7 weeks before SE to mark DGCs that had matured by the time of SE labeled cells wi

189 nes, Kruppel-like factor 9 (Klf9), in mature DGCs enhanced integration of adult-born DGCs and increas

190 tion by inducible deletion of Rac1 in mature DGCs increased survival of adult-born DGCs without affec

191 Reversal of Klf9 overexpression in mature DGCs restored spines and activity and reset neuronal com

192 st, DA suppressed MPP transmission to mature DGCs to a similar extent but did not influence their LTP

193 born DGCs are thought to compete with mature DGCs for inputs to integrate.

194 errant neuronal connections with neighboring DGCs, disrupting the dentate gate.

195 orary course of these alterations in newborn DGCs of female Tau(VLW) mice.

196 ned the dynamics of AIS formation in newborn DGCs of young female adult C57BL/6J mice in vivo Our dat

197 E) stimulates neurogenesis, but many newborn DGCs integrate aberrantly and are hyperexcitable, wherea

198 sed the morphological alterations of newborn DGCs and partially restored their connectivity in a mous

199 Eliminating cohorts of newborn DGCs by focal brain irradiation at specific times before

200 We studied establishment of newborn DGCs dendritic pattern and found it was mediated by a si

201 using single-cell transcriptomes of newborn DGCs, and among Golgi-related genes, found the presence

202 zation of the maturation dynamics of newborn DGCs, including their morphological development and the

203 ion of a key cellular compartment of newborn DGCs, namely, the axon initial segment (AIS) in vivo Our

204 pal dentate gyrus (DG) gives rise to newborn DGCs throughout the lifetime in rodents, we used RGB ret

205 No DGC- or PDE-encoding protein genes are present in the F.

206 No DGCs were labeled from an injection in the optic tectum.

207 iofilm formation by P. fluorescens Pf0-1, no DGCs from this strain have been characterized to date.

208 Treatments that restore normal DGC development after epileptogenic insults may therefor

209 status epilepticus (SE), whereas normotopic DGCs synapse onto both adult-born and early-born DGCs.

210 hey had not been previously exposed, a novel DGC population-rather than the previously activated DGC

211 muscle do not impact on the total amount of DGC components at the protein level.

212 ore age 50; families with 3 or more cases of DGC; families with 1 DGC before the age of 40; and famil

213 are all fundamental circuit determinants of DGC excitation, critical in both normal and pathological

214 bjects who had SRCC reported no diagnoses of DGC in first-degree relatives and did not meet establish

215 The effects of DGC gene mutations on phenotypes associated with biofilm

216 Expression of DGC components have been shown to be altered in many myo

217 a key factor in regulating the expression of DGC proteins at the sarcolemma.

218 Family history of DGC and endoscopic findings therefore do not appear to b

219 he age of 40; and families with a history of DGC and lobular breast cancer, with 1 diagnosis before t

220 viduals with and without a family history of DGC.

221 ariants in CDH1 who lack a family history of DGC.

222 s of CDH1 with and without family history of DGC.

223 The reported high incidence of DGC and limited sensitivity of endoscopy in detection ha

224 Our study reveals that the levels of DGC proteins at the sarcolemma differ in highly glycolyt

225 whether integrin compensates for the loss of DGC and UGC function in SSPN-nulls, we generated mice la

226 frequency-dependent synaptic recruitment of DGC activation in adult, but not developing, animals.

227 nd/or diatomic gas sensing and regulation of DGC activity.

228 CA3 pyramidal cells, the targets of DGC-derived mossy fibers, exhibited normal morphologies

229 phatase resulted in relocation of the AIS of DGCs without a depolarizing stimulus.

230 ot by alterations in afferent innervation of DGCs because GABA(A) antagonists normalized developmenta

231 The percentage of DGCs, as a proportion of all labeled cells, varied from

232 We found that both AB and EB populations of DGCs recorded from epileptic rats received increased exc

233 ynaptic inputs of age-defined populations of DGCs using electrophysiological recordings and fluoresce

234 ion potential firing in large populations of DGCs, we characterized the postnatal development of firi

235 abeled from nBOR, in which the proportion of DGCs was much higher (84-93%).

236 et DGCs discriminating between the I-site of DGCs and the active site of PDEs; this molecule represen

237 nducing proexcitatory changes in a subset of DGCs in isolation is sufficient to cause epilepsy in a r

238 whether adaptive changes in muscle impact on DGC expression.

239 One DGC preferentially affects LapA localization, another DG

240 ecurrent and widespread feedback loops, onto DGCs.

241 born DGCs without affecting proliferation or DGC activity.

242 With the exception of dystrophin, other DGC components were restored to the sarcolemma including

243 rn DGCs are targets of new inputs from other DGCs as well as from CA3 and CA1 pyramidal cells after p

244 of the A-site is also observed in many other DGCs.

245 hibit reduced excitability compared to other DGCs.

246 postnatal day (P)7] or adult-born (AB; P60) DGCs.

247 demonstrate that three of the five predicted DGC genes in E. amylovora (edc genes, for Erwinia diguan

248 ook a systematic mutagenesis of 30 predicted DGCs and found that mutations in just 4 cause reductions

249 tions, deletion of the two biofilm-promoting DGCs increased tissue necrosis in an immature-pear infec

250 Aergic responses in adolescent and adult rat DGCs are still depolarizing from rest.

251 Using a morphologically realistic DGC model, we show that GABAergic action, depending on i

252 leaves c-di-GMP to GMP and exhibits residual DGC activity.

253 This selection of a novel responsive DGC population could be triggered by small changes in en

254 se that PilY1 may act via regulation of SadC DGC activity but independently of altering global c-di-G

255 vo c-di-GMP concentration generated by seven DGCs, each expressed at eight different levels, to the c

256 Unlike wild type, a strain lacking all six DGCs did not exhibit a low-temperature-dependent increas

257 Of the 52 mutants tested, deletions of six DGCs and three PDEs were found to affect these phenotype

258 els via expression or activation of specific DGCs.

259 egulatory functions of c-di-GMP-synthesizing DGCs expand beyond surface attachment and biofilm format

260 al small molecule able to selectively target DGCs discriminating between the I-site of DGCs and the a

261 nd for future optimization studies to target DGCs in vivo.

262 g the interaction between dystrophin and the DGC and reveal that posttranslational modification of a

263 natal hearts deficient in both Hippo and the DGC showed cardiomyocyte overproliferation at the injury

264 ction between muscle fibre phenotype and the DGC.

265 ction between Hippo pathway function and the DGC.

266 In brain, the DGC is involved in the organisation of GABA(A) receptors

267 ly, CT alone was sufficient to establish the DGC at the sarcolemma.

268 progress in defining distinct roles for the DGC in neurons and glia.

269 Absence of alpha-syn from the DGC is known to lead to structurally aberrant neuromuscu

270 a model system to investigate if and how the DGC directly regulates the mechanical activation of musc

271 sed membrane residence of the integrins, the DGC/utrophin-glycoprotein complex of proteins and annexi

272 Expression of the DGC and UGC, laminin binding and Akt signaling were nega

273 Mutations in components of the DGC are responsible for muscular dystrophies and congeni

274 Our results support the dysregulation of the DGC at inhibitory synapses and altered neuronal network

275 dystrophin gene disrupt the structure of the DGC causing severe damage to muscle fibres.

276 ritical for the synaptic organization of the DGC in neurons remains elusive.

277 in which PTEN was deleted from >/= 9% of the DGC population developed spontaneous seizures in about 4

278 in 1 (InSyn1) is a critical component of the DGC whose loss alters the composition of the GABAergic s

279 To examine the functional role of the DGC, we expressed the Dp116 transgene in mice lacking bo

280 o promote the proteasomal degradation of the DGC.

281 effect of synaptically released GABA on the DGC population.

282 gulating HapR, and positively regulating the DGC Vca0939.

283 While R1-3 and R10-12 did not restore the DGC, surprisingly, CT alone was sufficient to establish

284 Here we show that the DGC component dystroglycan 1 (Dag1) directly binds to th

285 These data demonstrate that the DGC is critical for growth and maintenance of muscle mas

286 We conclude that the DGC promotes the mechanical activation of cardiac nNOS b

287 ed laterally from fibre to fibre through the DGC without decrement.

288 kable morphological similarities between the DGCs of Tau(VLW) mice and FTD patients.SIGNIFICANCE STAT

289 o CA3 pyramidal neurons, induces IGF2 in the DGCs.

290 These DGCs were characterized genetically and biochemically to

291 The proportion was small (2-3%), and these DGCs were smaller in size than those projecting to the n

292 increase in c-di-GMP, indicating that these DGCs are required for temperature modulation of c-di-GMP

293 ly controls swimming motility, while a third DGC affects both LapA and motility.

294 IGF2, in turn, localizes to DGC presynaptic terminals and stabilizes them in an acti

295 n individuals with genetic predisposition to DGC.

296 F. novicida strains lacking either the two DGC/PDE genes (cdgA and cdgB) or the entire gene cluster

297 nd efferent connectivity of newborn Tau(VLW) DGCs, and monosynaptic retrograde rabies virus tracing s

298 nts from retinal ganglion cells, but whether DGCs also project to LM remains unclear.

299 Association of InSyn1 with DGC subunits is required for InSyn1 synaptic localizatio

300 ial perforant path (MPP) inputs to the young DGCs, but also decreased their capacity to express long-