ライフサイエンスコーパス: katanin

1 altered with regard to their sensitivity to katanin.

2 5, and the microtubule-severing protein, p60/katanin.

3 which results in ubiquitin laddering of p60/katanin.

4 that regulate the severing properties of P60-katanin.

5 ubunits of the microtubule-severing complex, katanin.

6 ule severing enzymes, Spastin, Fidgetin, and Katanin.

7 axon lose their characteristic resistance to katanin.

8 related to the microtubule-severing protein katanin.

9 in vitro; thus, it is an ortholog of animal katanin.

10 eracted with the microtubule-severing enzyme KATANIN.

11 ce that microtubule severing is dependent on katanin.

12 ucleation sites until they become severed by katanin.

13 cruitment of the microtubule-severing enzyme katanin.

14 centrosome-associated WD repeat protein p80-katanin.

15 y subunit of the microtubule-severing enzyme Katanin.

16 subunits of the microtubule-severing ATPase katanin.

17 interacts with ciliary proteins and p60/p80 katanins.

18 Shotgun) and the microtubule-linked proteins Katanin-60, EB1, Milton and aPKC.

19 The microtubule-severing protein katanin, a heterodimer of 60 and 80 kDa subunits, was pr

20 Katanin, a heterodimer, consisting of catalytic (p60) an

21 as been observed in vitro to be catalyzed by katanin, a heterodimeric adenosine triphosphatase that c

22 Katanin, a member of the AAA adenosine triphosphatase (A

23 We show that C. elegans katanin, a microtubule severing AAA ATPase mutated in mi

24 equired after meiosis to negatively regulate katanin, a microtubule-severing complex, permitting the

25 Elements distal to the katanin AAA core sense alpha-tubulin tyrosination, and d

26 Recent work with purified spastin and katanin accounts for this phenotype by showing that, in

27 Katanin action is required both for normal alignment and

28 These findings reveal how Katanin activation is coupled to microtubule binding, th

29 Here, we demonstrate that katanin activity depends upon the behavior of the microt

30 plant cell wall since mutants with decreased katanin activity have been shown to have defective walls

31 zymes and suggest a scheme for regulation of katanin activity in cells dependent on free tubulin conc

32 We show that katanin activity is essential.

33 d in part by its absolute levels, given that katanin activity is high during mitosis.

34 any biological function, serve as sites for katanin activity.

35 s microtubule release under tight control of katanin activity.

36 Models that assumed that katanin acts on a uniform microtubule lattice were incom

37 itro data, whereas a model that assumed that katanin acts preferentially on spatially infrequent micr

38 p60 katanin, an AAA protein that severs and depolymerizes mi

39 ated by the evolutionary conserved proteins, KATANIN and CLASP.

40 function of spastin, as well as potentially katanin and fidgetin, are highly coordinated.

41 characterized family members, Vps4, spastin, katanin and fidgetin.

42 We modulated levels of katanin and intracellular calcium, two putative regulato

43 Comparison of katanin and kif2a phosphorylation sites across a variety

44 that the microtubule disassembling enzymes, katanin and kinesin-13 limit long-range movement of sper

45 Compound 5a directly targeted katanin and regulated the severing activity of katanin,

46 Two related enzymes, katanin and spastin, use the energy from ATP hydrolysis

47 urons with bFGF heightens expression of both katanin and spastin, which are proteins that sever micro

48 nt microtubule-severing proteins, namely P60-katanin and spastin.

49 lating the microtubule response to stress in katanin and spiral2 mutant made sepal shape dependent on

50 gnature, including the severases spastin and katanin and the microtubule regulators CRMP5 and tau, wa

51 urthermore, the microtubule-severing protein Katanin and the minus-end-binding protein Patronin accum

52 d this method to investigate the function of KATANIN and WRINKLED1 in cotton plant development.

53 ncludes the ATP-hydrolyzing enzymes spastin, katanin, and fidgetin, which sever microtubule polymers

54 remodelers comprises the severases-spastin, katanin, and fidgetin-which cut microtubules into shorte

55 KATNB1 with KATNA1, the catalytic subunit of Katanin, and other microtubule-associated proteins.

56 reviously identified MT destabilizers (Op18, katanin, and XKCM1/KinI).

57 protein that is recognized by an anti-human katanin antibody and that this protein is localized, at

58 s of neurons that had been injected with the katanin antibody compared with controls.

59 mplexes is significantly blocked by the anti-katanin antibody.

60 In contrast, Katanin appears to function primarily on anaphase chromo

61 ctors ARF7/ARF19, auxin influx carriers, and katanin are dispensable for apical hook formation, indic

62 tions in hereditary spastic paraplegias, and katanin are related microtubule-severing AAA ATPases inv

63 Spastin and P60-katanin are two distinct microtubule-severing proteins.

64 e identified the microtubule-severing enzyme katanin as a central player in controlling the organizat

65 dopsis thaliana depends on their severing by katanin at crossovers.

66 Microtubules are severed by katanin at distinct cellular locations to facilitate reo

67 is activated during meiosis, phosphorylates Katanin at multiple serines.

68 phorylation at the other sites only inhibits Katanin ATPase activity stimulated by MTs.

69 table protection of the microtubules against katanin-based loss.

70 ules through both a spastin-based mode and a katanin-based mode.

71 vide correspondingly less protection against katanin-based severing.

72 microtubule dynamics by the severing enzyme KATANIN became vital when XyGs were perturbed or absent.

73 New evidence suggests that katanin - best known for severing microtubules in their

74 ntify the effect of katanin concentration on katanin binding and severing activity.

75 nhibit severing activity by interfering with katanin binding to microtubules.

76 ere, we report that p80-like(MEI-2) dictates Katanin binding to MTs via two MTBDs composed of basic p

77 Substituting these patches reduces Katanin binding to MTs, compromising its function in fem

78 The mechanism by which spastin and katanin break and destabilize microtubules is unknown, i

79 nal growth is sensitive to the levels of P60-katanin, but that other factors contribute to modulating

80 We also find that katanin can remove tubulin dimers from the ends of MTs,

81 tion mutations in the Caenorhabditis elegans katanin catalytic subunit, MEI-1, cause specific defects

82 e characterized the N-terminal domain of the katanin catalytic subunit.

83 s the noncatalytic regulatory p80 subunit of katanin, cause severe microlissencephaly.

84 e spiral of electropositive loops lining the katanin central pore.

85 MEI-1 may ensure temporal activation of the katanin complex during meiosis, whereas CRL3(MEL-26)-med

86 subunit (p80) in providing MT binding to the Katanin complex.

87 We quantify the effect of katanin concentration on katanin binding and severing ac

88 final levels of severing, and sensitivity to katanin concentration over the range 6-300 nM.

89 We find that severing activity depends on katanin concentration.

90 Expression of a dominant-negative P60-katanin construct in cultured neurons inhibits microtubu

91 we show that the microtubule-severing enzyme katanin contributes to hook formation.

92 Furthermore, katanin deficiencies phenocopy a mutation of beta-tubuli

93 We found that katanin-dependent MT severing was increased in X. tropic

94 increasing microtubule density and a second, katanin-dependent phase that occurs after microtubule de

95 We show that D-spastin, like katanin, displays ATPase activity and uses energy from A

96 n of branches, whereas overexpression of P60-katanin does not.

97 Consistent with this finding, GFP-tagged katanin driven by its native promoter localizes at sites

98 ediate the spindle-pole assembly activity of katanin during female meiosis.

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

100 a mutation in the p80 regulatory subunit of katanin, encoded by the PF15 gene in Chlamydomonas, alte

101 Katanin exhibits graded and divergent responses to gluta

102 Cotton plants with suppressed KATANIN expression produced shorter fibers and elevated

103 mology domain protein encoded by aspm-1, the katanin family member mei-1, and the kinesin-12 family m

104 KATNAL2, a member of Katanin family microtubule-severing ATPases, is a known

105 ase and Katanin p60-like 1 (Kat-60L1) of the Katanin family of microtubule severing proteins are requ

106 t of an E3 ubiquitin ligase complex, targets katanin for degradation during the transition from meios

107 Oligomerization increased the affinity of katanin for microtubules and stimulated its ATPase activ

108 esidue is necessary and sufficient to target Katanin for proteasomal degradation after meiosis, where

109 Overexpression of katanin for short periods of time produced breaks prefer

110 How katanin fulfills its controlling role, however, remains

111 rotubule-binding domains (MTBD) required for Katanin function in C. elegans.

112 Notably, interference with katanin function prevented structural spine remodeling f

113 Recent work on spastin and katanin has partially resolved this paradox by showing t

114 tubule-severing proteins, p56, EF1alpha, and katanin, has only confused the issue because none of the

115 to encode a protein with high similarity to katanin (hence FRA2 was renamed AtKTN1), a protein shown

116 The katanin hexamer central pore constrains the polyglutamat

117 The microtubule templates katanin hexamerization and activates its ATPase.

118 In Caenorhabditis elegans, the katanin homologue MEI-1 is required for meiosis, but mus

119 on with antibodies specific for a vertebrate katanin homologue to demonstrate that katanin is respons

120 KATNB1 encodes a subcomponent of katanin, important in maintaining microtubule homeostasi

121 roblasts to be more resistant to severing by katanin in a manner that was not dependent on the acetyl

122 otubule-anchoring complex is used to recruit katanin in acentrosomal plant cells.

123 and activity of the MT-severing protein p60-katanin in interneurons to promote the rapid remodeling

124 ound that consistent with a critical role of katanin in mitosis, constitutive homozygous Katna1 deple

125 The role of p60 katanin in the mammalian brain with respect to embryonic

126 -1 and its activator PPFR-1 ensure efficient katanin inactivation in the transition to mitosis.

127 was degraded after meiosis, contributing to katanin inactivation.

128 spindle shortening proceeds through an early katanin-independent phase marked by increasing microtubu

129 We found that purified katanin induced an ATP-dependent severing of the Chlamyd

130 Katanin inhibition lengthened spindles in both species.

131 Furthermore, katanin inhibition reduced the invasion of microtubules

132 Here we show that p60/katanin interacts with a complex consisting of Cul3 and

133 Katanin is a conserved AAA ATPase with the ability to se

134 Katanin is a heterodimeric enzyme that severs microtubul

135 Katanin is a heterodimeric microtubule-severing protein

136 Katanin is a heterohexamer of dimers containing a cataly

137 Katanin is a microtubule-severing complex whose catalyti

138 Katanin is a microtubule-severing enzyme that is concent

139 Katanin is a neuronally expressed microtubule-severing c

140 Studying mice from both sexes, we found that katanin is abundant in neuronal dendrites and can be det

141 Katanin is abundant in oocytes, and its levels drop afte

142 To determine whether katanin is also required for spindle maintenance, we mon

143 Katanin is an evolutionarily conserved microtubule (MT)-

144 Katanin is broadly distributed in the neuron, and theref

145 mmunofluorescence analysis demonstrated that katanin is concentrated at a microtubule-dependent struc

146 microtubule (MT)-severing AAA-ATPase enzyme Katanin is emerging as a critical regulator of MT dynami

147 The microtubule-severing enzyme katanin is essential for plants to form aligned microtub

148 esults indicate that microtubule-severing by katanin is essential for releasing microtubules from the

149 rotubules at the centrosome, indicating that katanin is indeed required for microtubule release from

150 P60-katanin is more highly expressed in the neuron, but spas

151 When katanin is overexpressed in fibroblasts, the microtubule

152 es on cultured sympathetic neurons show that katanin is present at the centrosome, but is also widely

153 Katanin is recruited to these sites for efficient releas

154 that sensitivity to microtubule severing by katanin is regulated by a balance of factors, including

155 e sensitivity of microtubules to severing by katanin is regulated by acetylation of the microtubules.

156 This suggests that katanin is regulated in part by its absolute levels, giv

157 Previous work showed that katanin is required for severing at points where two mic

158 This result suggests that katanin is responsible for changes in microtubules occur

159 ebrate katanin homologue to demonstrate that katanin is responsible for the majority of M-phase sever

160 We conclude that katanin is solely responsible for severing at CMT crosso

161 ation of microtubule dynamics often involves KATANIN (KTN): a microtubule severing enzyme that cuts m

162 The microtubule-severing enzyme katanin (KTN1) regulates the organization and turnover o

163 sphorylation and dephosphorylation fine-tune Katanin level and activity to deliver the appropriate MT

164 Similarly, in neuronal cultures, katanin levels are high when axons are allowed to grow a

165 Using various rat tissues, we found that P60-katanin levels are much higher than spastin levels durin

166 In the adult, P60-katanin levels plunge dramatically but spastin levels de

167 rodent brain, neurons vary significantly in katanin levels, depending on their developmental stage.

168 HDC5-deficient cells show an increase in p60/katanin levels, indicating that Cul3/Ctb9/KLHDC5 is requ

169 Taken together, these data suggest that a katanin-like mechanism may mediate the severing of the o

170 These results indicate that the katanin-like protein is essential for oriented cellulose

171 We further demonstrated that the Arabidopsis katanin-like protein possessed MT-severing activity in v

172 gether, these results suggest that AtKTN1, a katanin-like protein, is essential not only for normal c

173 responsible for the fra2 mutation encodes a katanin-like protein.

174 Strikingly, katanin localizes and severs at the interface of GMPCPP-

175 found in adult mouse brain, indicating that katanin may have other functions distinct from its mitot

176 Our data demonstrate that katanin-mediated microtubule severing regulates structur

177 r in size to X. tropicalis but that TPX2 and katanin-mediated scaling is not conserved.

178 crotubules for a fixed pool of tubulin, with katanin-mediated severing allowing easier access to this

179 loped to enable the real-time observation of katanin-mediated severing of individual, mechanically un

180 ed that phototropin photoreceptors stimulate katanin-mediated severing specifically at microtubule in

181 er the microtubule-severing protein known as katanin mediates microtubule release from the neuronal c

182 n complex is the microtubule-severing enzyme katanin (MEI-1).

183 In Caenorhabditis elegans, the MEI-1-katanin microtubule-severing complex is required for mei

184 microtubules and then dissociated into free katanin monomers.

185 eric protein phosphatase 4 complex, enhanced katanin MT-severing activity during C. elegans meiosis.

186 In Caenorhabditis elegans, Katanin MT-severing activity is essential for meiotic sp

187 owed that CMTs fail to become ordered in the katanin mutant.

188 was completely abolished in the Arabidopsis katanin mutant.

189 titative imaging experiments and analysis of katanin mutants showed that the longitudinal arrays are

190 h a delay in the fate restriction process in katanin mutants.

191 r assay demonstrated that the p60 subunit of katanin oligomerized in an adenosine triphosphate (ATP)-

192 After hydrolysis of ATP, microtubule-bound katanin oligomers disassembled microtubules and then dis

193 The net effect of katanin on the polymer mass depends on the microtubule t

194 Depletion of katanin or double depletion of kinesin-13 and ataxin-2 r

195 Depletion of either katanin or spastin with siRNA diminished but did not eli

196 required for transport) pathway and spastin, katanin p60 and fidgetin affecting multiple aspects of c

197 ks an inhibitory phosphorylation site in the katanin p60 catalytic subunit.

198 Katanin p60 haploinsufficiency induced an accumulation o

199 al role for the microtubule-severing protein katanin p60 in regulating neuronal progenitor proliferat

200 nown regarding the role of the family member Katanin p60 subunit A-like 1, KATNAL1, in central nervou

201 IS1 homology (LisH) motif, including several katanin p60 subunits, muskelin, tonneau, LEUNIG, Nopp140

202 Katanin p60 was the first ATPase associated with microtu

203 irement for the microtubule-severing protein katanin p60-like 1 (Kat-60L1) in regulating the elaborat

204 Here, we show that both the Ik2 kinase and Katanin p60-like 1 (Kat-60L1) of the Katanin family of m

205 rogression through ubiquitination of phospho-katanin p60.

206 In this work, we investigate how katanin (p60), believed to be the first discovered sever

207 We demonstrate unequivocally that Katanin phosphorylation at a single residue is necessary

208 ics in C. elegans and deciphered the role of Katanin phosphorylation in the regulation of its activit

209 red that microtubule severing by the protein katanin plays a crucial and unexpected role in the reori

210 We propose that katanin preferentially severs older, post-translationall

211 During chromosome segregation, WDR62 and katanin promote efficient poleward microtubule flux and

212 lators of deciliation, and found that excess katanin promotes cilia loss by deciliation, independentl

213 bules renders them notably less sensitive to katanin, prompting us to posit that microtubule disinteg

214 ERH3 encodes a p60 katanin protein that is expressed throughout the plant.

215 These results indicated that katanin protein, but not katanin's microtubule-severing

216 Katanin proteins are known to sever microtubules, and ha

217 881) show that microtubule severing by katanin provides a means for increasing microtubule dens

218 emonstrate that Msd1-Wdr8 acts as a specific katanin recruitment factor to cortical nucleation sites

219 We also show that katanin reduces the levels of several types of post-tran

220 Although katanin reduces the polymer mass and destabilizes the in

221 ry role of the N-terminal domain of MEI-1 in Katanin regulation.

222 butyrophilin subfamily 2 member A1 (BTN2A1), katanin regulatory subunit B1 (KATNB1), and transmembran

223 The katanin regulatory subunit in turn caused a dramatic cha

224 necessary and sufficient for binding to the katanin regulatory subunit.

225 rt a model in which MBK-2 down-regulates the katanin-related protein MEI-1 to control spindle positio

226 l3/Ctb9/KLHDC5 is required for efficient p60/katanin removal.

227 croinjection of an antibody that inactivates katanin results in a dramatic accumulation of microtubul

228 Overexpression of wild-type P60-katanin results in excess microtubule severing and is al

229 f short microtubules, whereas the excess P60-katanin results in short microtubules intermingled with

230 ant MT orientation caused by the mutation of katanin results in the distorted deposition of cellulose

231 These results indicate katanin's activities are segregated into a subunit (p60)

232 Given Katanin's evolutionary conservation, our work provides a

233 To determine the relationship between katanin's microtubule-severing activity and its role in

234 ults indicated that katanin protein, but not katanin's microtubule-severing activity, is required for

235 activity of the microtubule severing protein katanin scales the X. tropicalis spindle smaller compare

236 Here, we investigate the activity of katanin severing using a GFP-labeled human version.

237 We thus propose a mechanism whereby Katanin-severing at the single active centrosome release

238 It may be that katanin severs microtubules throughout the cell body to

239 The AAA ATPase katanin severs microtubules.

240 We show that inhibition of katanin slows the rate of spindle shortening in nocodazo

241 Microtubule-severing enzymes (MSEs), such as Katanin, Spastin, and Fidgetin play essential roles in c

242 Microtubule-severing enzymes - katanin, spastin, fidgetin - are related AAA-ATPases tha

243 udy using electron tomography has found that katanin stimulates the production of microtubules in the

244 veral oocyte proteins, including the meiotic katanin subunit MEI-1 and the oocyte maturation protein

245 sion of a dominant-negative ATPase-deficient katanin subunit to functionally inhibit severing alters

246 In mbk-2 mutants, the meiosis-specific katanin subunits MEI-1 and MEI-2 persist during mitosis

247 e report the sequences and activities of the katanin subunits.

248 ification of dynamic microtubule arrays, but katanin targeting mechanisms are poorly understood.

249 rongly shield them from being severed by P60-katanin than by spastin.

250 n the axon are more resistant to severing by katanin than microtubules elsewhere in the neuron.

251 nstrate a novel regulatory mechanism for p60/katanin that occurs at the level of targeted proteolysis

252 In dividing cells, the levels of P60-katanin (the subunit with severing properties) increase

253 e severing protein that shares homology with katanin, the microtubule severing activity of which prom

254 Katanin, the microtubule-severing protein, consists of a

255 s of the microtubule-severing protein termed katanin to completely break down the axonal microtubule

256 the sufficient and necessary conditions for katanin to promote array alignment, stresses the critica

257 ivalent microtubule recognition that enables katanin to read multiple tubulin modification inputs exp

258 sordered region outside the AAA core anchors katanin to the microtubule while the AAA motor exerts th

259 mportant because tau regulates the access of katanin to the microtubule.

260 onal microtubules against excess severing by katanin, under conditions of tau depletion.

261 The microtubule-severing enzyme katanin uses ATP hydrolysis to disrupt noncovalent bonds

262 Surprisingly, katanin was also found in adult mouse brain, indicating

263 The microtubule-severing subunit p60 of katanin was identified as a candidate substrate for MAB1

264 nsitivity of the microtubules to severing by katanin was increased or decreased, respectively.

265 To understand the nonsevering activities of katanin, we characterized the N-terminal domain of the k

266 nd functional similarity between spastin and katanin, we hypothesized that spastin promotes the dynam

267 Using Caenorhabditiselegans Katanin, which contains the MEI-1 catalytic AAA+ p60 and

268 tanin and regulated the severing activity of katanin, which cut the cellular microtubules into short