ライフサイエンスコーパス: C. elegans

1 C. elegans expressing only WDR-23A display activation of

2 C. elegans G protein-coupled receptors have been implica

3 C. elegans has also become a model for parasitic nematod

4 (C. elegans hermaphrodites are somatic females that trans

5 C. elegans hermaphrodites display dramatic age-related d

6 C. elegans makes RQ and can use RQ-dependent metabolic p

7 C. elegans MALT-1 forms a complex with homologs of Act1

8 C. elegans offers a powerful model for identifying such

9 A C. elegans model of tauopathy reveals that A152T and A15

10 We show that neurons in a C. elegans sensory organ, called the amphid, undergo a c

11 reduce its associated toxicity in vivo in a C. elegans worm model expressing Abeta42.

12 MEX-5 (Muscle EXcess) is a C. elegans protein that leads a cascade of RBP localizat

13 We show that a C. elegans one-cell stage centrosome at metaphase contai

14 86 +/- 0.35 mum diameter cell) compared to a C. elegans embryo (5.78 +/- 0.18 mum(2) in a 55.83 +/- 1

15 Here, using a C. elegans circuit of interneurons that are connected by

16 d somatic and synaptic compartments in adult C. elegans with fluorescent proteins, and isolated synap

17 Thus, adult C. elegans males employ a neuroendocrine feedback loop t

18 rmation, and pathogenesis in a P. aeruginosa-C. elegans infection model.

19 We discovered that, after C. elegans have learned to avoid the pathogenic bacteria

20 rains cultured from such rotting fruit allow C. elegans growth and reproduction when tested individua

21 Here we show that feeding state alters C. elegans thermotaxis behavior by engaging a modulatory

22 nimal models, such as mouse, Drosophila, and C. elegans, have revealed many exciting principles of th

23 s parent H6 to human cardiac fibroblasts and C. elegans.

24 Here, we show that GCNA mutants in mouse and C. elegans display defects in genome maintenance includi

25 w KLP11/20 kinesin-2 from C. reinhardtii and C. elegans through a DNA tether to understand the molecu

26 Another C. elegans terminal selector (UNC-30/Pitx) also exhibits

27 he N2 assembly has many differences from any C. elegans available today.

28 ual small biological model organisms such as C. elegans or isolated single cells have been limited by

29 ignal transduction pathway conserved between C. elegans and mammalian cells to enable the transcripti

30 RNAi and drug screens and in systems beyond C. elegans embryos.

31 In both C. elegans and human cancer cells, ether-lipid synthesis

32 divisions, cell size changes rapidly in both C. elegans and zebrafish [2, 3], where mitotic centrosom

33 The flexible escape behavior exhibited by C. elegans in response to threats relies on a combinatio

34 Within the thermal range experienced by C. elegans, the population of the unfolded state of the

35 ism of stem cell niche exit in the canonical C. elegans distal tip cell (DTC) germ stem cell niche me

36 ctly activated by DAF-16/FoxO, the canonical C. elegans IIS effector.

37 viruses have been isolated from wild-caught C. elegans (Orsay virus) and its relative Caenorhabditis

38 atform analysis in Saccharomyces cerevisiae, C. elegans, and Xenopus laevis, we present studies ident

39 complete, excluding the time spent culturing C. elegans, and includes (i) experimental design and pre

40 Regeneration of laser-cut C. elegans neurons requires early action of core apoptos

41 conditions of increased population density, C. elegans animals prolong the duration of reproductive

42 m specification varies widely among distinct C. elegans wild isotypes, owing to rapid developmental s

43 We use Drosophila, C. elegans and D. rerio to show that, although both expr

44 precursor cell (AC/VU) fate decision during C. elegans gonadogenesis, two "alpha cells," each with e

45 ndle assembly and chromosome dynamics during C. elegans female meiosis.

46 However, it has been suggested that during C. elegans female meiosis, anaphase is mediated by a kin

47 l analysis of par-1 gene expression in early C. elegans embryos.

48 ng cell division and Caenorhabditis elegans (C. elegans) growth.

49 tage of the nematode Caenorhabditis elegans (C. elegans).

50 y, we report a new assay format for engaging C. elegans in burrowing that enables rapid assessment of

51 These results establish C. elegans as a powerful animal model to study the induc

52 x-specific features are static: for example, C. elegans males (XO) can sometimes exhibit hermaphrodit

53 th rate and reproduction in chitosan exposed C. elegans.

54 on developmental gene expression dataset for C. elegans from Bao, Murray, Waterston et al. to gain in

55 endogenous synthesis of LA is essential for C. elegans development.

56 In screens for C. elegans responses to single bacterial strains associa

57 utonomous signaling in modulating aging from C. elegans to mammals.

58 tode species estimated to have diverged from C. elegans 280 to 430 million y ago.

59 We discuss evidence from C. elegans and murine/human systems supporting the conce

60 ced body muscle-specific transcriptomes from C. elegans lacking functional dystrophin at distinct sta

61 uced pheromone sensitivity across the global C. elegans population.

62 Our data reveal how C. elegans utilizes nuclear receptors to regulate innate

63 s, we demonstrate that, similarly to humans, C. elegans is able to synthesize LA de novo via a lipoyl

64 ress/immune program in C. elegans IMPORTANCE C. elegans lacks homologs of most mammalian pattern reco

65 In C. elegans oocytes and embryos, SEIP-1 is associated wit

66 In C. elegans the netrin receptor UNC-40/DCC controls the g

67 In C. elegans, biological sex and feeding state regulate ex

68 In C. elegans, deletion of AMPK or of key autophagy and mit

69 In C. elegans, expression of the UPR(ER) transcription fact

70 In C. elegans, iron uptake and sequestration are regulated

71 In C. elegans, nuclear-localized small RNAs engage the nucl

72 In C. elegans, piRNAs are transcribed from > 15,000 discret

73 In C. elegans, PUF-8 binds to an 8-nt motif and restricts p

74 In C. elegans, sexual maturation of the nervous system incl

75 In C. elegans, the roles of the PAR proteins in embryonic d

76 In C. elegans, this transition is marked by the appearance

77 lex (SC) through phosphorylation of SYP-1 in C. elegans.

78 e evidence for transcriptional adaptation in C. elegans, a powerful model to further investigate unde

79 Here we report transcriptional adaptation in C. elegans, and find that this process requires factors

80 SYD-2 is the homolog of liprin-alpha in C. elegans known to activate UNC-104; however, signals t

81 undance in mammalian cells in culture and in C. elegans neurons in vivo Inhibition of the proteasome

82 ary to maintain ER integrity in yeast and in C. elegans.

83 certain modifications to the ascarosides in C. elegans, instead activates the side chains of certain

84 ve model of future proliferation behavior in C. elegans based on a snapshot of CDK activity in newly

85 hannel required for sodium chemosensation in C. elegans, but its specific role remains unclear.

86 nly one RFX factor regulates ciliogenesis in C. elegans, several distinct RFX factors have been impli

87 e capable of driving chromatin compaction in C. elegans.

88 tribute to X Chromosome-wide condensation in C. elegans hermaphrodites.

89 During many stages and conditions in C. elegans, sleep requires a sleep-active neuron called

90 over, tyrosine fragmentation is conserved in C. elegans.

91 Here we show that, in its natural context in C. elegans, RDE-3 adds pUG tails to targets of RNA inter

92 nd ECM degradation-mediated muscle damage in C. elegans.

93 both result in a nuclear anchorage defect in C. elegans.

94 are structure- and composition-dependent in C. elegans.

95 chrony of the early embryonic development in C. elegans is determined independently by individual cel

96 APK pathway to promote larval development in C. elegans.

97 ) Essentially all somatic sex differences in C. elegans are governed by the master regulator tra-1, w

98 asis of centrosome strength and ductility in C. elegans embryos.

99 Here we analyzed Katanin dynamics in C. elegans and deciphered the role of Katanin phosphoryl

100 inding site by CRISPR-Cas9 genome editing in C. elegans We developed a multiplexed negative selection

101 generation through the ARF activator Efa6 in C. elegans, and by neurodevelopmental disorders linked t

102 We observed the same effects in C. elegans demonstrating the conservation of this self-d

103 on adr-2, the sole A-to-I editing enzyme in C. elegans However, we also identified a subset of neura

104 fining a mechanism of longevity extension in C. elegans-bacterial colonization, innate immune activat

105 h comprise a greatly expanded gene family in C. elegans Here we use coimmunoprecipitation studies pai

106 romote proper ovulation and fertilization in C. elegans.

107 We found in C. elegans that GABAergic motor neurons (D-MNs) bias tow

108 of mcp-1, the single homologue of GDPGP1 in C. elegans, leads to increased degeneration of GABA neur

109 ur-alpha, as a component of germ granules in C. elegans We show that PLP-1 is essential for silencing

110 Indeed, studies of short-term habituation in C. elegans indicate that in this paradigm, multiple gene

111 We show here in C. elegans that nitric oxide derived from resident bacte

112 RO function and carboxylesterase homologs in C. elegans and other animals may reveal additional new c

113 some, a distinctive feature of anaphase I in C. elegans males, is due to lack of chromosome pairing.

114 ellular factors impacting viral infection in C. elegans and humans.

115 homology) domain rescued Orsay infection in C. elegans, demonstrating conservation of its function t

116 in understanding glia-neuron interactions in C. elegans.

117 ce of these observations was investigated in C. elegans by transgenic expression of conserved UNC-45

118 te healthspan and lifespan investigations in C. elegans.

119 ch suggests that neuroectoderm involution in C. elegans is potentially homologous with vertebrate neu

120 omotes thermotolerance as part of the IPR in C. elegans, which adds to our understanding of how organ

121 o critically examine putative cases of it in C. elegans.

122 Our results indicate that dnc-1 KD in C. elegans is a useful model for the screening of drugs

123 elicits a marked increase of SUMO levels in C. elegans.

124 ntal chromosomes at the beginning of life in C. elegans and possibly also in humans, where a defect i

125 ing in restoration of health and lifespan in C. elegans under high glucose and other stress condition

126 translation is known to increase lifespan in C. elegans, and is accompanied by a fragmented mitochond

127 loss of cell adhesion activates lysosomes in C. elegans epidermis during developmental remodeling of

128 uired for TMC-1-mediated mechanosensation in C. elegans OLQ neurons and body wall muscles.

129 as a dual rRNA and tRNA methyltransferase in C. elegans mitochondria.

130 e on condensed chromosomes during mitosis in C. elegans embryos.

131 ghput analysis of oxidative modifications in C. elegans.

132 and evaluate their role in sperm motility in C. elegans, we developed a novel biochemical method for

133 modes of piRNA organization in nematodes: in C. elegans and closely related nematodes, piRNAs are clu

134 yeast and dopaminergic neurodegeneration in C. elegans.

135 WC(ON), a well-described olfactory neuron in C. elegans, here we derive a general and broadly useful

136 e identify the insulin signalling pathway in C. elegans and interventions altering bacterial physiolo

137 expenditure via DAF-12-dependent pathway in C. elegans.

138 f the cholinergic motor neuron called PDB in C. elegans.

139 ll transcriptomes to their exact position in C. elegans' invariant lineage.

140 Therefore, the role of PP2A in C. elegans female meiosis is unknown.

141 ral behaviors and physiological processes in C. elegans hermaphrodites [2-5].

142 to activate the IPR stress/immune program in C. elegans IMPORTANCE C. elegans lacks homologs of most

143 es and spontaneous genomic rearrangements in C. elegans.

144 ated version of the only insulin receptor in C. elegans has been discovered.

145 at function downstream of IL-17 receptors in C. elegans neurons.

146 ged 29 BM matrix components and receptors in C. elegans with mNeonGreen.

147 spine-like protrusions have been reported in C. elegans (Philbrook et al., 2018), suggesting that the

148 1 in directing a transcriptional response in C. elegans called the intracellular pathogen response (I

149 th and target specificity of nuclear RNAi in C. elegans, ensuring faithful inheritance of epigenetic

150 From a genetic screen in C. elegans, we found that pix-1 is required for the asse

151 first performed large-scale drug screens in C. elegans which uncovered 74 hits.

152 From genetic screens in C. elegans, we identified splicing factor RNP-6/PUF60 wh

153 ore during meiotic chromosome segregation in C. elegans oocytes has been a matter of controversy.

154 ify a network that stabilizes cell shapes in C. elegans embryos at a stage that involves non-autonomo

155 Here, we show in C. elegans that disrupting mitochondrial network homeost

156 E opening surrounding the meiotic spindle in C. elegans oocytes.

157 tion at the level of alternative splicing in C. elegans that parallels the evolutionary forces and co

158 ues across different developmental stages in C. elegans.

159 functional representation of sexual state in C. elegans is neither static nor homogeneous, challengin

160 e for molecular and toxicological studies in C. elegans.

161 The flip-flop sleep switch in C. elegans thus requires an additional component, wake-a

162 f GABA(A) receptors at GABAergic synapses in C. elegans The interaction of N-MADD-4B with NLG-1 is al

163 at both exogenous and endogenous targets in C. elegans.

164 cal, and behavioral evidence showing that in C. elegans an ortholog of the human LAT1 transporter, AA

165 We show that in C. elegans morphogenesis, apical constriction in the ret

166 Here, we show that in C. elegans not only is H3K9me3 unnecessary for inheritan

167 Our results suggest that in C. elegans, dystrophin may have a signaling role early i

168 We achieve this in C. elegans by engineering a multicolor transgene called

169 Thus, in C. elegans alternative splicing at the daf-2 locus gener

170 iously implicated in developmental timing in C. elegans, contributes to temporal accumulation of TRA-

171 pendent alphaSyn aggregation and toxicity in C. elegans models and prevents alphaSyn-mediated vesicle

172 e 5-fluoro 2'deoxyuridine (FUdR) toxicity in C. elegans through different microbial mechanisms.

173 1 acts as a regulator of EGFR trafficking in C. elegans.

174 reases in ROS decrease calcium transients in C. elegans glutamatergic neurons.

175 tal progression and cell-fate transitions in C. elegans larvae under stress so that the developmental

176 e, remaining life and lifespan of individual C. elegans.

177 vivo biofilms, in the persistently infected C. elegans gut.

178 C. elegans (ExCel), to expand fixed, intact C. elegans.

179 ivo imaging of AMPAR transport in the intact C. elegans nervous system, we demonstrate that long-dist

180 ptic stochasticity in an otherwise invariant C. elegans cell lineage.

181 to convey learned avoidance of PA14, and its C. elegans target, maco-1, is required for avoidance.

182 evidence that it is secreted, similar to its C. elegans ortholog (OIG-4) [10].

183 t tcer-1 promotes longevity in germline-less C. elegans and reproductive fitness in wild-type animals

184 ate of the intracellular environment in live C. elegans worms.

185 output is significantly lower in long-lived C. elegans daf-2 mutants.

186 ultaneous quantification of each of the main C. elegans motor programs over hours or days.

187 le nutrients in a completely defined medium (C. elegans maintenance medium [CeMM]), specifically gluc

188 s were tested in vivo using the animal model C. elegans.

189 Moreover, C. elegans gcna-1 mutants are hypersensitive to TOP2 poi

190 in promoting extended healthspan of multiple C. elegans tissues, underscore the potency of early exer

191 xpression of wild-type NLG-1 in nlg-1 mutant C. elegans rescued their sensory and learning impairment

192 ughput mRNA sequencing of these prp-8 mutant C. elegans reveals that overall alternative splicing pat

193 ram, in response to infection by the natural C. elegans viral pathogen Orsay virus.

194 avioral flexibility using the model nematode C. elegans.

195 the distinct motor programs of the nematode C. elegans are coupled together across behavioral states

196 Here, we show that in the nematode C. elegans, a neurotransmitter-sensing G protein-coupled

197 monstration, namely neurites in the nematode C. elegans, but are applicable to other systems and tran

198 In the nematode C. elegans, insulin signaling regulates development and

199 matic sexual differentiation in the nematode C. elegans, where it was reported to be expressed sex-sp

200 physiologic, and behavioral abnormalities of C. elegans.

201 O(2) beads affected the food availability of C. elegans, with greater effects by the PS beads.

202 Using the egg-laying circuit of C. elegans as a model, we mapped which cells express eac

203 mmetries in the locomotion neural circuit of C. elegans, each characterized by its own symmetry group

204 at the complete set of 118 neuron classes of C. elegans can be described individually by unique combi

205 e lethal in combination with a collection of C. elegans mutations that disrupt particular iron-sulfur

206 these models in the developmental context of C. elegans embryogenesis, we undertook chromosome tracin

207 ur data indicate that the bacterial diets of C. elegans provide precisely tailored amounts of iron to

208 ExM of C. elegans is challenged by its cuticle, which is stiff

209 Here we present a strategy, expansion of C. elegans (ExCel), to expand fixed, intact C. elegans.

210 Here we show that the function of C. elegans Slo2 (SLO-2) depends on adr-1, a gene importa

211 The recompleted genome of C. elegans should be a valuable resource for genetics, g

212 s play a central role in the life history of C. elegans and other nematodes; however, many aspects of

213 efficient chemical exchange for hundreds of C. elegans embryos simultaneously.

214 c pipeline for large-scale smFISH imaging of C. elegans embryos with minimized labor.

215 only used and represent strong indicators of C. elegans fitness, there is an increasing need to repla

216 actor essential for Orsay virus infection of C. elegans Ablation of HIPR-1 resulted in a greater than

217 inally, we demonstrate that wild isolates of C. elegans display variation in seam cell sensitivity to

218 ing compounds, by increasing the lifespan of C. elegans up to 16.82%, 16.65%, 16.53%, and 12.93%, res

219 The chemosensory BAG neurons of C. elegans are striking exemplars of this.

220 ntly alter the structure and organization of C. elegans sarcomeres.

221 d for measuring the metabolic heat output of C. elegans.

222 d higher antioxidant capacity, protection of C. elegans from ROS generation, and soluble solid conten

223 wed that UNC-3/Ebf, the terminal selector of C. elegans cholinergic motor neurons (MNs), acts indirec

224 ces of dauer individuals from six strains of C. elegans to the preferences of other life stages.

225 Studies of C. elegans have been particularly influential because th

226 evelopmental polyadenylated transcriptome of C. elegans Taking advantage of long reads spanning the f

227 ple egg-laying circuit in the model organism C. elegans We identified all the cells that express ever

228 of signaling molecules in the model organism C. elegans.

229 ity status of genes for two model organisms (C. elegans and S. cerevisiae) using the GenAge database

230 nd that upon exposure to P. aeruginosa PA14, C. elegans undergoes a rapid loss of intact ribosomes ac

231 In a screen for mutations protecting C. elegans from hypoxic stress, we isolated multiple gen

232 inescent Escherichia coli strain to quantify C. elegans feeding.

233 cription factor, NHR-23/NR1F1, in regulating C. elegans molting, we discovered that NHR-23/NR1F1 is a

234 estigate collective feeding in the roundworm C. elegans at this intermediate scale, using quantitativ

235 The roundworm C. elegans reversibly arrests larval development during

236 Systemic depletion of hsp-17 shortens C. elegans lifespan and severely reduces fecundity and s

237 nt with a potential role in Notch signaling, C. elegans ubr-7 expression partially overlaps with that

238 me-resolved metabolic measurements of single C. elegans worms from larval to adult stages.

239 ETS-5 targets revealed that NHR-6, the sole C. elegans NR4A-type nuclear receptor, is required for B

240 -tunes DAF-16 and SKN-1 activity in specific C. elegans somatic tissues, to enhance stress resistance

241 curs but is delayed, and progeny of stressed C. elegans mothers fail to complete development.

242 in contrast to most rodent in vivo studies, C. elegans assays provide well-defined concentration-res

243 We demonstrate that C. elegans EFHC-1 functions within specialized non-motil

244 We further find that C. elegans colonized by Providencia preferentially selec

245 report that C. elegans CED-3 caspase promotes animal growth through

246 Here, we show that C. elegans mRNA decay factors, including the translation

247 Here, we show that C. elegans PIR-1 dephosphorylates ppp-RNAs made by cellu

248 Additionally, we show that C. elegans sleep can be induced through mechanosensory p

249 We show that C. elegans synMuv B proteins regulate developmental chro

250 organization of the connectome suggests that C. elegans has some similarities with encoder-decoder ar

251 The C. elegans scaffold protein KRI-1, ortholog of mammalian

252 ced stress response regulated by atfs-1, the C. elegans ortholog of ATF4, causing hypersensitivity to

253 Mutants lacking KIN-29, the C. elegans homolog of a mammalian Salt-Inducible Kinase

254 We approach the C. elegans connectome as an information processing netwo

255 quiescence (PRQ), which is modulated by the C. elegans response to cellular stressors.

256 essor of AdipoR2 knockdown, thus echoing the C. elegans findings.

257 We report a role for the C. elegans separase SEP-1, primarily known for its essen

258 Here, we have identified the C. elegans zinc finger transcription factor PQM-1 as a r

259 pping of primordial germ cells (PGCs) in the C. elegans embryonic gonad primordium.

260 assembly of P granules, RNA granules in the C. elegans germ plasm.

261 sion at defined chromosomal locations in the C. elegans germline and show that the position of the re

262 nsgenerational epigenetic inheritance in the C. elegans germline.

263 siRNAs in controlling gene expression in the C. elegans germline.

264 rsity of intermediate filaments (IFs) in the C. elegans intestine indicate important contributions to

265 d with previously described mutations in the C. elegans lifespan and stress-response pathways.

266 MALT-1 is expressed broadly in the C. elegans nervous system, and neuronal IL-17-MALT-1 sig

267 Centrosomes break symmetry in the C. elegans one-cell embryo, triggering its anterior-post

268 ables cholinergic motor neurons (MNs) in the C. elegans ventral nerve cord to select and maintain the

269 demonstrate that the glial cells of the C. elegans amphid apparatus serve as odorant receptor ce

270 proach) to constitute the "rich-club" of the C. elegans connectome.

271 Growth of the C. elegans dynamin mutant on an Escherichia coli strain

272 eability barrier, the innermost layer of the C. elegans embryonic eggshell.

273 ting the temporo-spatial organisation of the C. elegans germline and time-resolved methods of protein

274 Fam151b is a mammalian homologue of the C. elegans menorin gene, which is involved in neuronal b

275 er, coordinate sexual differentiation of the C. elegans nervous system.

276 e report that decreasing the function of the C. elegans torsinA homolog, OOC-5, rescues the sterility

277 of both Ubr1 and Ubr2 in the mouse or of the C. elegans UBR5 ortholog results in Notch signaling defe

278 in-coupled receptor required to regulate the C. elegans response to infection with Microbacterium nem

279 We show that the C. elegans RIG-I homolog DRH-1 mediates the induction of

280 nveloping endotube, which is attached to the C. elegans apical junction.

281 mplex that is lethal in combination with the C. elegans mitochondrial mutations.

282 robactin are not synthetic lethal with these C. elegans mitochondrial mutants; it is the enterobactin

283 Analogous to C. elegans, the response of CHORDC1-deficient A431 cells

284 While some strains were highly sensitive to C. elegans and the nematode pheromone ascarosides, other

285 the utilization of the genetically tractable C. elegans model will provide a key resource for dissect

286 We have established a transgenic C. elegans line, expressing the human D76N beta(2)-m var

287 B and alpha-synuclein toxicity in transgenic C. elegans models correlated with the prolongation of MT

288 Of the two C. elegans enzymes that require B12, gene inactivation o

289 ed sup-45 as one of the two hitherto unknown C. elegans orthologs of the human AF4/FMR2 family protei

290 -dependent metabolic pathways - here, we use C. elegans genetics to show that tryptophan degradation

291 Here we use C. elegans whole genome sequencing to systematically qua

292 We used C. elegans to study how mechanisms that sense environmen

293 By using C. elegans as a genetic model, we could visualize mitoch

294 eriments support a great potential for using C. elegans to model SEIPIN-associated human diseases.

295 studies lysosomal degradation pathways using C. elegans as a model system.

296 and viral pathogens, the mechanisms by which C. elegans recognizes these pathogens have remained some

297 However, in the temperature range in which C. elegans is fertile, when MEX-5 needs to be functional

298 sembly and define Nigon elements shared with C. elegans, which we then map to the genomes of other fi

299 Epistasis studies with C. elegans daf-2 mutants showed that mir-228 and mir-235

300 Additionally, past studies with C. elegans provide evidence that the nematode's innate b