ライフサイエンスコーパス: autophagosome

1 o the delivery of p62 and its cargoes to the autophagosome.

2 proteins to allow growth and closure of the autophagosome.

3 ed to encapsulate autophagic cargo within an autophagosome.

4 f VZV particles housed in a double-membraned autophagosome.

5 formed from the fusion of an endosome and an autophagosome.

6 contents into a double-membrane vesicle, the autophagosome.

7 f-eating by a double-membrane organelle, the autophagosome.

8 called the phagophore that matures into the autophagosome.

9 entriolar satellites colocalize with forming autophagosomes.

10 uitment and defective formation of canonical autophagosomes.

11 ve LC3, suggesting that they originated from autophagosomes.

12 mentin cage independent of MAP1LC3B positive autophagosomes.

13 ntation, disorganised cristae, and increased autophagosomes.

14 response by localizing ER-resident STING to autophagosomes.

15 malian target of rapamycin with LC3-positive autophagosomes.

16 sicles; viral particles were not observed in autophagosomes.

17 ron microscopy we identified double-membrane autophagosomes.

18 omal dysfunction and impaired degradation of autophagosomes.

19 , which led to the association of TRAF6 with autophagosomes.

20 AB11-positive recycling endosomes to forming autophagosomes.

21 ysosomes for degradation via double-membrane autophagosomes.

22 rom the axon combined with locally generated autophagosomes.

23 livered to lysosomes for degradation through autophagosomes.

24 )P and promoting actin nucleation at nascent autophagosomes.

25 positively regulates RAB7 recruitment to LE/autophagosomes.

26 n its host cells, including the induction of autophagosomes.

27 ght to act as a membrane carrier for forming autophagosomes.

28 The autophagosome, a double-membrane structure mediating deg

29 c constituents, leading to generation of the autophagosome, a double-membrane vesicle, which is targe

30 erol, a major component of lipid rafts, from autophagosomes abolished HCV RNA replication.

31 e interaction of Sec24 with Atg9 to increase autophagosome abundance.

32 Here we show that autophagosomes accumulate due to impaired fusion with ly

33 LIV pathology, including the contribution of autophagosome accumulation to muscle dystrophy and the r

34 FLT3-ITD molecules were detectable within autophagosomes after bortezomib treatment indicating tha

35 ses, including endosome formation, fusion of autophagosomes/amphisomes with lysosomes, and apoptosis.

36 rane trafficking and remodelling to form the autophagosome and deliver its contents to lysosomes for

37 her small GTPase, Rab2, is also required for autophagosome and endosome maturation and proper lysosom

38 biogenesis, loss of all Atg8s yields smaller autophagosomes and a slowed initial rate of autophagosom

39 duced LC3-II formation and a lower number of autophagosomes and autolysosomes during both basal and s

40 ated using electron microscopic detection of autophagosomes and by measuring LC3B protein lipidation

41 tion increased the formation of LC3-positive autophagosomes and degradation of cargo both in human ce

42 gy, in which mitochondria are sequestered by autophagosomes and delivered to lysosomes for degradatio

43 developed a procedure to purify HCV-induced autophagosomes and demonstrated that HCV could induce th

44 hesize that CFS1 acts at the intersection of autophagosomes and endosomes and contributes to cellular

45 acid receptor-associated protein (GABARAP)+ autophagosomes and endosomes.

46 aneously monitoring different populations of autophagosomes and identified 34 out of 186 Rab GTPase,

47 8 (PNPLA8) gene, and PNPLA8 associates with autophagosomes and is associated with a decrease in cell

48 n-binding protein that aggregates protein in autophagosomes and is degraded upon autophagy that was r

49 njugation system in mediating the closure of autophagosomes and its implication in the study of autop

50 is caused by perturbed delivery of cargo via autophagosomes and late endosomes to SiNP-filled catheps

51 Rab7 promotes fusion of autophagosomes and late endosomes with lysosomes in yeas

52 ation promoted clearance of Tau oligomers by autophagosomes and lysosomes.

53 s that trigger the coordinated biogenesis of autophagosomes and lysosomes.

54 horous vacuole (PV) by directing fusion with autophagosomes and lysosomes.

55 vacuolar compartment or VAC) in turnover of autophagosomes and persistence during neural infection.

56 SQSTM1 can bind to LC3 on autophagosomes and ubiquitinated molecules on cargos, th

57 ysosomal fusion reactions essential for LDL, autophagosome, and macropinosome degradation.

58 the formation of double-membrane autophagic autophagosomes, and this process is operational in airwa

59 n of double-membrane-bound structures called autophagosomes (AP), which engulf material to be degrade

60 We show that fewer autophagosomes are generated in the NAP1 knockout mutant

61 Altogether, our results indicate that autophagosomes are key organelles to help avoid C99 accu

62 raded by lysosomes, mitochondrion-containing autophagosomes are released from the cell.

63 vity, and proximal tubular mitochondrial and autophagosome area and number (by transmission electron

64 ates or bulk cytoplasm, respectively, inside autophagosomes as cargo for delivery to lysosomes.

65 Additionally, our studies reveal that autophagosomes associate with FAs primarily during disas

66 The soma, however, contains autophagosomes at different maturation states, including

67 as localized in the cell nuclei, ~30% was in autophagosomes/autophagolysosomes and the remainder was

68 d that the rest of the DNA can be cleared by autophagosomes/autophagolysosomes.

69 nd most or all of the rest of the DNA was in autophagosomes/autophagolysosomes.

70 tion of SNARE priming, the initial stages of autophagosome biogenesis and autophagosome expansion rem

71 that both of these proteins cause increased autophagosome biogenesis and compromised lysosomal activ

72 We observe autophagosome biogenesis in the axon near synapses, and

73 Neurons are highly polarized cells in which autophagosome biogenesis is spatially compartmentalized.

74 taining vesicles is considered a key step in autophagosome biogenesis, aided by Atg1 complexes (ULK1

75 centrosome occurs during starvation-induced autophagosome biogenesis, but how centrosomal proteins r

76 berrant Atg8 puncta and drastically impaired autophagosome biogenesis, leading to severe defects in n

77 h neither GABARAPs nor LC3s are required for autophagosome biogenesis, loss of all Atg8s yields small

78 the ATG4 protease, an essential protein for autophagosome biogenesis, plays a central role for the r

79 mainly in yeast, including the mechanism of autophagosome biogenesis, the function of the core macro

80 s as a modulator of macroautophagy, inducing autophagosome biogenesis.

81 as a modest increase in LC3-IIB, a marker of autophagosome biogenesis.

82 n of Atg9 and COPII vesicles at the start of autophagosome biogenesis.

83 pro-LC3 and the de-lipidation of LC3-PE from autophagosomes, both executed by the same cysteine prote

84 ubsequently disseminates from the cell in an autophagosome-bound mitochondrion-virus complex.

85 bules when in tight association with forming autophagosomes, but independently of the mitochondrial d

86 is replicates both in the cytosol and within autophagosomes, but the bacteria failed to replicate whe

87 protein FUNDC1 interacts with LC3 to recruit autophagosomes, but the mechanisms integrating these pro

88 eins are attached to the membrane of nascent autophagosomes, but their functions during autophagy are

89 romises autophagy at the maturation stage of autophagosomes by interacting with Beclin 1/Rab7 and dys

90 ysis of proteins associated with HCV-induced autophagosomes by proteomics led to the identification o

91 esult in reduced processing of the excessive autophagosomes by the rate-limiting lysosomal activity.

92 on and maturation of the phagophore into the autophagosome, by facilitating the recruitment of the At

93 Moreover, there was evidence of impaired autophagosome clearance after chloroquine administration

94 reased glucocerebrosidase activity, impaired autophagosome clearance by the lysosome, and decreased m

95 also demonstrate that RAB2A is required for autophagosome clearance in human breast cancer cells.

96 hanistic explanation for the coordination of autophagosome completion and fusion with the vacuole.

97 Here, we found that accumulation of autophagosomes compromised cell viability, and this effe

98 93A)), we show that motor neurons form large autophagosomes containing ubiquitinated aggregates early

99 Autophagosomes cooperate in the degradation of intracell

100 entrosomal GABARAP reservoir, and centrosome-autophagosome crosstalk.

101 we show that CCT integrity is essential for autophagosome degradation in cells or Drosophila and thi

102 osomes in many cellular functions, including autophagosome degradation, cholesterol homeostasis, anti

103 state, the cell soma contains populations of autophagosomes derived from distinct neuronal compartmen

104 Finally, mature autophagosomes detach from the ER membrane by an as yet

105 tly unfused to lysosomes (or accumulation of autophagosomes) directly induces cellular toxicity, and

106 ave been implicated as a membrane source for autophagosomes, distinct organelles that engulf cellular

107 as specifically required for the assembly of autophagosomes downstream of LC3II processing.

108 we showed recently that vaccines composed of autophagosomes (DRibbles) derived from syngeneic sarcoma

109 Hence, TBC1D5 shuttling to autophagosomes during metabolic stress facilitates retro

110 We propose that the acute need to produce autophagosomes during starvation drives the interaction

111 The urgent need for membranes to form autophagosomes during starvation to maintain homeostasis

112 d ultrastructural characteristics typical of autophagosomes during the late stage of infection.

113 Here, we compare autophagosome dynamics within neuronal compartments.

114 ngly, the autophagy product ATG5 involved in autophagosome elongation positively regulated TG2/NF-kap

115 f Atg5, an E3 ubiquitin ligase essential for autophagosome elongation, in macrophages impaired the re

116 breakdown of mitochondrial inner membranes, autophagosome enclosure of paternal mitochondria, and PM

117 s a significant increase in puncta of LC3(+) autophagosomes, endogenous levels of LC3-II, and ultrast

118 Axonal autophagosomes enter the soma and remain confined within

119 at mammalian cells are capable of generating autophagosomes even without it.

120 itial stages of autophagosome biogenesis and autophagosome expansion remain resistant to its loss.

121 c components by multilayered vesicles called autophagosomes, followed by lysosomal fusion and degrada

122 condary receptor to assist RIG-I delivery to autophagosomes for degradation in a p62-dependent manner

123 ABARAP proteins, targeting mitochondria into autophagosomes for degradation.

124 volving its I35 and F52 residues, to recruit autophagosomes for execution of lethal mitophagy.

125 y induce the association of lipid rafts with autophagosomes for its RNA replication.IMPORTANCE HCV ca

126 isolated inside specialized vesicles called autophagosomes for recycling and degradation.

127 ine that, in Caenorhabditis elegans neurons, autophagosomes form near synapses and are required for n

128 onse, whereas chronic alcohol exposure slows autophagosome formation along with an elevation of gut-d

129 n 1, known to play an important role in both autophagosome formation and autolysosome fusion, in indu

130 rfering RNA-mediated WNK1 knockdown, we show autophagosome formation and autophagic flux are accelera

131 ith ATG8, a ubiquitin-like protein directing autophagosome formation and cargo recruitment.

132 PCM1 enhances GABARAP/WIPI2/p62-positive autophagosome formation and flux but has no significant

133 DAC cells, chemotherapeutic agents triggered autophagosome formation and increased LC3 expression thr

134 in ubiquitin binding, was also defective in autophagosome formation and recruitment to the Atg12-5-1

135 Ulk1 activation augmented autophagosome formation and reduced autophagy flux.

136 We show that Atg8s are dispensable for autophagosome formation and selective engulfment of mito

137 anes, where they have been proposed to drive autophagosome formation and selective sequestration of c

138 distinct pathways that coordinately initiate autophagosome formation at the yeast vacuole.

139 t LC3/GABARAP proteins are not essential for autophagosome formation but are critical for autophagoso

140 phosphorylation at Ser-177 was required for autophagosome formation but not for Optn recruitment to

141 ective hepatocytes was not due to defects in autophagosome formation but was due to impairment of lip

142 We also found that inhibition of autophagosome formation by depletion of Atg5 led to high

143 KIF1A/UNC-104 coordinates localized autophagosome formation by regulating the transport of t

144 athway directly and indirectly contribute to autophagosome formation during starvation.

145 IL-6 stimulates LC3 conversion and autophagosome formation in cultured beta cells.

146 lated 7 (Atg7) and Atg16L1 and the status of autophagosome formation in the hippocampus of immature r

147 y inhibiting Atg7 and Atg16L1 expression and autophagosome formation in the hippocampus.

148 asmic proteasome puncta that accumulate when autophagosome formation is blocked.

149 Autophagosome formation is complex: initiated by the rec

150 Our findings provide key insights into how autophagosome formation is regulated by a novel negative

151 A fundamental question is how autophagosome formation is regulated.

152 pharmacologic treatments that either inhibit autophagosome formation or block the fusion of autophago

153 Autophagosome formation requires sequential translocatio

154 that ULK1, a protein kinase activated at the autophagosome formation site, phosphorylates human ATG4B

155 ATG4B stimulates autophagy by promoting autophagosome formation through reversible modification

156 e fusion, in induction of LC3II, a marker of autophagosome formation, and in induced degradation of p

157 d conversion of LC3B-I to LC3B-II, decreased autophagosome formation, and increased p62 level compare

158 lly tethers ER and mitochondria also reduces autophagosome formation, and that this artificial tether

159 In contrast, activation of autophagosome formation, either by starvation or by inhi

160 nt in isolation membrane (or phagophore) and autophagosome formation, maturation, or autophagosome-ly

161 d with ATG8-family-specific functions during autophagosome formation, on residues absent in the LC3 f

162 of the cellular sites believed to engage in autophagosome formation, review basic mechanisms used to

163 ecause AP1S3 encodes a protein implicated in autophagosome formation, we next investigated the effect

164 as Orencia), demonstrated reduced levels of autophagosome formation, while DCs from CTLA4-Ig-treated

165 the autophagy receptor optineurin (Optn) in autophagosome formation.

166 PB or PTPIP51 to loosen contacts stimulates, autophagosome formation.

167 autophagosomes to allow cargo selection and autophagosome formation.

168 domain, and ATG9A vesicles together initiate autophagosome formation.

169 autophagosomes and a slowed initial rate of autophagosome formation.

170 response to mitochondrial depolarization and autophagosome formation.

171 s host autophagy protein ATG8CL to stimulate autophagosome formation.

172 in protein HS1BP3 is a negative regulator of autophagosome formation.

173 ociated OPTN or TBK1 mutant blocks efficient autophagosome formation.

174 t has no significant effect on LC3B-positive autophagosome formation.

175 d abnormal bulk autophagy despite unimpaired autophagosome formation.

176 ubpopulation of damaged lysosomes to promote autophagosome formation.

177 on with Atg14L and reduces Beclin1-dependent autophagosome formation.

178 t chain 3-II (LC3-II), which is required for autophagosome formation.

179 orylation of Unc-51-like kinase 1 (ULK1) and autophagosome formation.

180 ed brain injury attenuation through inducing autophagosome formation.

181 urons after SE, together with an increase in autophagosome formation.

182 ruitment of downstream autophagy factors and autophagosome formation.

183 the phagophore assembly site (PAS), where an autophagosome forms, at a very early stage of autophagy,

184 n that was accompanied by increased podocyte autophagosome fractional volume and p62 aggregation, whi

185 Forming the autophagosome from the phagophore, a cup-shaped double-m

186 Autophagosomes from cells lacking GABARAPs had reduced l

187 inity chromatography for the purification of autophagosomes from cells that harbor an HCV subgenomic

188 recycling, thereby preventing endosomes and autophagosomes from reaching lysosomes.

189 erization is necessary for the biogenesis of autophagosomes from the endoplasmic reticulum (ER) membr

190 During early infection, autophagosomes fuse with ehrlichial vacuoles to form an

191 In contrast, autophagosomes generated in Rab5-null mutant cells norma

192 In contrast, autophagosomes generated within the soma are less mobile

193 The purified autophagosomes had double- or multiple-membrane structur

194 Autophagosomes have associated PIPKIgammai5 and PtdIns(4

195 axonal transport of dense core vesicles and autophagosomes in a PP2A-dependent fashion.

196 Recent studies established that nascent autophagosomes in distal axons move predominantly in the

197 gosome marker ATG8, and anti-NAP1 identifies autophagosomes in immuno-TEM.

198 dition, electron microscopy showed increased autophagosomes in rod inner segments with HDAC inhibitor

199 Thus, the excessive autophagosomes in such situations may be largely unfused

200 ated substrates in an expanded population of autophagosomes in the absence of greater autophagy induc

201 ased the number of EGFP-LC3 cells expressing autophagosomes in the cytoplasm.

202 e was preceded by accumulation of undigested autophagosomes in the parasite cytoplasm.

203 s specific to HCV, as it was not detected in autophagosomes induced by nutrient starvation.

204 We found that autophagosome initiation and maturation by TGFbeta is de

205 nent of the autophagy machinery required for autophagosome initiation.

206 n of IBTKalpha helps prevent accumulation of autophagosome intermediates stemming from exposure to sa

207 Thus, the autophagosome is a flexible membrane platform with dimen

208 Atg proteins are translocated to the forming autophagosome is not fully understood.

209 The autophagosome is thought to nucleate from vesicles conta

210 noparticles were localized within macrophage autophagosomes, leading to a 4-fold enhancement of mitoc

211 agy, manifested by an accumulation of sealed autophagosomes located in close proximity to lysosomes b

212 Functioning lysosomes are required for autophagosome-lysosomal fusion in the autophagy pathway.

213 s in the first intron of genes that regulate autophagosome/lysosomal degradation, mitochondrial traff

214 2 in podocytes and the importance of TFEB to autophagosome-lysosome function in these cells.

215 as recently emerged as a master regulator of autophagosome-lysosome function, controlling the express

216 regulation of syntaxin 17, a SNARE promoting autophagosome-lysosome fusion and cargo degradation.

217 has an antiamyloidogenic function, promoting autophagosome-lysosome fusion and increasing betaCTF deg

218 Second, CYCLO impeded autophagosome-lysosome fusion as evidenced by the accumu

219 ic capacity but has no significant effect on autophagosome-lysosome fusion or autolysosomal clearance

220 lso demonstrated that IBDV infection induced autophagosome-lysosome fusion, but without active degrad

221 us the Ccz1-Mon1-Rab7 module is required for autophagosome-lysosome fusion, whereas Rab5 loss interfe

222 ily promotes PLEKHM1 recruitment and governs autophagosome-lysosome fusion, whereas the LC3 subfamily

223 retrograde lysosomal transport and prevents autophagosome-lysosome fusion.

224 ngulfment of mitochondria, but essential for autophagosome-lysosome fusion.

225 autophagosome formation but are critical for autophagosome-lysosome fusion.

226 and autophagosome formation, maturation, or autophagosome-lysosome fusion.

227 tant CSPalpha cause a block in the fusion of autophagosomes/lysosomes.

228 Importantly, partial depletion of autophagosome machinery proteins Atg16L1 and Beclin 1 si

229 d this effect was alleviated by depletion of autophagosome machinery proteins.

230 estingly, the majority co-localizes with the autophagosome marker ATG8, and anti-NAP1 identifies auto

231 ased colocalization of mitochondria with the autophagosome marker LC3B.

232 ulation of lipidated light chain 3 (LC3), an autophagosome marker, by Western blotting and confocal f

233 NOD1 promoted pro-IL-1beta restriction and autophagosome maturation arrest, while NOD2 promoted cas

234 y suppression of PI3K and potentiated by the autophagosome maturation blocker bafilomycin.

235 d interference with cellular membrane fusion/autophagosome maturation could have unfavorable conseque

236 accumulated regulators of late endosome (LE)/autophagosome maturation.

237 e of stereocilia structure, endocytosis, and autophagosome maturation.

238 By slowing substrate delivery to lysosomes, autophagosome maturational delay, as further confirmed b

239 Therefore, lowering the accumulation of autophagosomes may represent a therapeutic strategy for

240 iquitin (UB)-like proteins conjugated to the autophagosome membrane and are thought to facilitate car

241 and the questions relating to the sources of autophagosome membrane(s).

242 milieu, gangliosides are constituents of the autophagosome membrane, a subset of proteins composing t

243 RAP) that are intimately associated with the autophagosome membrane.

244 The motor protein dynein drives autophagosome motility from distal sites of assembly to

245 vae administered ALA + DFO showed hepatocyte autophagosomes, nuclear membrane ruffling, and porphyrin

246 linositol-3-kinase complexes responsible for autophagosome nucleation.

247 g autophagy, Sec24 phosphorylation regulates autophagosome number and its interaction with the C-term

248 hanced gut-derived LPS decreases the hepatic autophagosome numbers in response to alcohol exposure, a

249 Increased autophagosome numbers, expression of lysosomal cathepsin

250 We propose that the nucleation of autophagosomes occurs in regions, where the ULK1 complex

251 on co-expressed beclin-1 or LC3, markers for autophagosome or autophagolysosome formation, and perili

252 CL-2, and BCL-XL through the accumulation of autophagosomes, p62, and JNK signaling.

253 is mediated via the p-eIF2alpha rather than autophagosome pathway.

254 ating the PA content of the ATG16L1-positive autophagosome precursor membranes through PLD1 activity

255 autophagy, via uptake into ATG16L1-positive autophagosome-precursor vesicles.

256 3 is localized to ATG16L1- and ATG9-positive autophagosome precursors and we show that HS1BP3 binds p

257 n complex translocates to the ATG9A-positive autophagosome precursors in a PI3P-dependent manner.

258 ine TG neurons triggered unusual clusters of autophagosomes, predominantly in neurons lacking detecta

259 Further analysis indicated that the autophagosomes purified from HCV replicon cells could me

260 nally, serine 34/35 phosphorylation enhances autophagosome recruitment to mitochondria in HeLa cells.

261 gy-related SNARE protein syntaxin17 with the autophagosome remained unaffected.

262 The role of cytotoxicity in accumulating autophagosomes (representing synthesis of autophagosomes

263 hich function in maturation and formation of autophagosomes, respectively.

264 Punctate LC3B and autophagosomes staining confirmed autophagy.

265 data suggest that production/accumulation of autophagosomes subsequently unfused to lysosomes (or acc

266 ng autophagosomes (representing synthesis of autophagosomes subsequently unfused to lysosomes) has no

267 Autophagy comprises the processes of autophagosome synthesis and lysosomal degradation.

268 We tested whether reduction in autophagosome synthesis could affect cell viability in c

269 In certain stress conditions, increased autophagosome synthesis may be associated with decreased

270 ATG14 contains a C-terminal Barkor/ATG14(L) autophagosome-targeting sequence (BATS) domain that sens

271 mine (PE) on the inner and outer membrane of autophagosomes to allow cargo selection and autophagosom

272 tophagosome formation or block the fusion of autophagosomes to endolysosomal compartments caused an i

273 pairs FA turnover and decreases targeting of autophagosomes to FAs, whereas ectopic expression of aut

274 ggest that FoxO3 stimulates the formation of autophagosomes to increase autophagic capacity but has n

275 by delivering cytosolic material captured by autophagosomes to lysosomes for degradation.

276 ld induce the localization of lipid rafts to autophagosomes to mediate its RNA replication.

277 double- or multiple-membrane vesicles termed autophagosomes to remove protein aggregates and damaged

278 onnector of kinase to AP-1) as essential for autophagosome transport in neurons.

279 intenance of axonal growth-cone dynamics and autophagosome turnover.

280 ributes to cellular homeostasis by mediating autophagosome turnover.

281 TT patients display a defective formation of autophagosomes under conditions of nutrient starvation a

282 eads to a rapid increase in the formation of autophagosomes, unique organelles that replenish the cel

283 hat, in DC, specific targeting of HIV Ags to autophagosomes using a microtubule-associated protein L

284 and other short-lived proteins (SLiPs) into autophagosomes via sequestosome (SQSTM1, p62) mediated a

285 Their association with autophagosomes was also confirmed in HCV-infected cells.

286 association of lipid rafts with HCV-induced autophagosomes was confirmed by Western blotting, immuno

287 The association of lipid rafts with autophagosomes was specific to HCV, as it was not detect

288 ogether, these data support a model in which autophagosomes were directed to the LDs via SQSTM1, whic

289 novo formation of a new organelle called the autophagosome, which either surrounds and sequesters ran

290 a de novo double-membrane vesicle termed the autophagosome, which matures by fusing to the lysosome.

291 in a transient double-membrane organelle, an autophagosome, which subsequently fuses with a lysosome

292 Thus, Trib3 was required for formation of autophagosomes, which accumulated in neurons as autophag

293 of cytoplasmic components in double-membrane autophagosomes, which are delivered to lysosomes for deg

294 pendent recruitment of Rab7 to PI3P-positive autophagosomes, which are generated by the action of the

295 Internalized MOG colocalized with autophagosomes, which can protect from destructive proce

296 of LC3-II(+) cytosolic structures resembling autophagosomes, which seem to form an intracellular comp

297 rough the assembly, transport, and fusion of autophagosomes with lysosomes for degradation.

298 SNARE Syntaxin 17 to modulate the fusion of autophagosomes with lysosomes.

299 or Atg31, leads to a defect in the fusion of autophagosomes with the vacuole and decreased autophagy

300 gen species, leading to sequestration by the autophagosome within approximately 45 min after insult.