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1 actin as controlled by Cofilin, Anillin, and Septin.
2 terface mutant as the sole source of a given septin.
3 skeletal components, including the four core septins.
4 the molecular basis of curvature sensing by septins.
5 ng a latent "holdase" activity toward mutant septins.
6 sites drive curvature-specific adsorption of septins.
7 he results demonstrate a stimulatory role of septin-2 and the dynamic reorganization of septin oligom
9 ith tandem MS and immunoblot analyses of the septin-2 interactome in mouse brain, we identified not o
11 306 and forced expression of a non-cleavable Septin-2 restored cytokinesis, suggesting a direct mecha
12 Among binding partners, NS2B-NS3 cleaved Septin-2, a cytoskeletal factor involved in cytokinesis.
13 to the SNARE complex, did not interact with septin-2, indicating that septins undergo reorganization
14 ural and thermodynamic properties of a human septin 3 construct, SEPT3-GC, which contains both of bot
16 uper-resolution imaging of ORAI1, STIM1, and septin 4 in living cells that septins facilitate Ca(2+)
23 In this issue, Bridges et al. discover that septins, a component of the cytoskeleton, recognize memb
24 aries as cells stretch into damaged regions, septins accumulate at the wound margin, and intermediate
25 -to-double-ring transition in budding yeast, septins acquire a "zonal architecture" in which paired s
26 ce homodimerization by a GTPase-active human septin also creates hexamers that exclude Cdc10-like cen
28 t report of an arginine finger observed in a septin and suggests that CrSEPT may act as its own GTP-a
29 the first evidence of an interaction between septins and a nonmitotic kinesin and suggest that SEPT9
32 tional appressoria and does not organize the septins and polarity determinants that are required for
34 s until after bud emergence, suggesting that septins and/or Hsl7 respond to a "bud sensor." Here we s
35 ical or aging-associated diminishment of the septin/anillin-scaffold causes myelin outfoldings that i
36 ccepted during this process, the function of septins, another cytoskeletal component that associates
37 ssential roles of a RhoGEF-anillin module in septin architectural remodeling during cytokinesis at th
38 y illustrates how a protein kinase regulates septin architecture at the filament level and suggests t
63 perresolution imaging, we show that Hof1 and septins are patterned at the bud neck into evenly spaced
70 ropose that guanidinium reactivates a latent septin assembly pathway that was suppressed during funga
71 findings explain how GTP hydrolysis controls septin assembly, and uncover mechanisms by which cells c
72 (ANLN) from oligodendrocytes disrupts myelin septin assembly, thereby causing the emergence of pathol
73 show that different regions of Gps1 and the septin-associated kinase Gin4 are involved in maintainin
74 ed of two tandem, semiredundant but distinct septin-associating elements, is necessary and sufficient
75 een shown by other means to bind directly to septins at the bud neck in vivo, we validate that the tr
76 se results suggest that Hof1, while bound to septins at the bud neck, not only regulates Bnr1 activit
81 affinity for the C-terminal domains of human septins belonging to the SEPT6 and SEPT7 groups (SEPT6C/
82 UMOylation sites to the C-terminal domain of septins belonging to the SEPT6 and SEPT7 groups and to t
84 to analyze the biophysical properties of the septin-binding protein Bni5 and how its association with
86 the SEPT6 and SEPT7 groups leads to aberrant septin bundle formation and defects in cytokinesis after
87 tion of septin-GFP molecules incorporated in septin bundles in growing hyphae of a filamentous fungus
89 death that are associated with dysregulated septin cage-like formation, impaired autophagic p62/LC3
93 t Saccharomyces cerevisiae, the five mitotic septins (Cdc3, Cdc10, Cdc11, Cdc12, and Shs1) localize t
94 crotubule-membrane interaction, depending on septins, Cdc42, Borgs, and restructuring of the actin cy
99 1-950, efficient localization of Hsl1 to the septin collar in the cell obligatorily requires generali
102 ur data support that Gef3 interacts with the septin complex and activates Rho4 GTPase as a Rho GEF fo
103 We reconstituted a recombinant Drosophila septin complex and compared activities of the wild-type
104 recognition complex (ORC), directly binds to septin complex and facilitates septin filament formation
105 vide a functional dissection of a Drosophila septin complex and highlight the basic conserved and div
109 h to sense curvature, as we find that single-septin complexes have curvature-dependent association ra
110 ited our previous work in which we generated septin complexes in which all endogenous cysteine (Cys)
111 specific meiotic and mitotic subunits endow septin complexes with functionally distinct properties.
122 tance using Ca(2+) chelator and inhibitor of septin cytomatrix in morphologically diverse synapses.
128 letion or pharmacologic stabilization of the septin cytoskeleton significantly inhibited NK cell cyto
129 recognition is a fundamental property of the septin cytoskeleton that provides the cell with a mechan
131 en membranes and the actin, microtubule, and septin cytoskeletons, these studies highlight the membra
134 xocyst complex at the appressorium pore is a septin-dependent process, which also requires regulated
135 for the organization of microtubules and for septin-dependent remodeling of the F-actin cytoskeleton
136 Appressorium-mediated infection requires septin-dependent reorientation of the F-actin cytoskelet
137 his second checkpoint specifically regulates septin-dependent, NADPH oxidase-regulated F-actin dynami
139 at pre-patterns two cytokinetic structures-a septin double ring and an actomyosin ring-and also defin
141 letion of septin-2 by siRNA or impairment of septin dynamics by forchlorfenuron inhibited constitutiv
144 egulation of SEPT9 or chemical inhibition of septin filament assembly impairs recruitment of MMP3 to
145 modeling which allowed us to determine that septin filament assembly was a diffusion-driven process,
149 s coordinated process is crucial for correct septin filamentation and efficient growth of polarised c
152 ts the known spacing between the subunits in septin filaments and thus serves as a "molecular ruler."
154 polymers to stay associated with membranes, septin filaments do not have to span micrometers in leng
155 G2/M transition unless and until a collar of septin filaments has properly assembled at the bud neck,
157 Previously we identified the assembly of septin filaments in the innermost non-compacted myelin l
158 roach also was used to follow the binding to septin filaments of a septin-interacting protein, the ty
160 nd negative micrometric radii of curvatures, septin filaments remain straight and perpendicular to th
161 e suggest that anillin-dependent assembly of septin filaments scaffolds mature myelin sheaths, facili
162 quire a "zonal architecture" in which paired septin filaments that are organized along the mother-bud
163 The model captures the reorganizations of septin filaments throughout cytokinesis in vivo, providi
166 d axis associate with circumferential single septin filaments, the Rho guanine-nucleotide-exchange fa
168 report that, after cleavage furrow closure, septins form a membrane-bound double ring that controls
178 methods for image analysis, we investigated septin function during pheromone-dependent chemotropic g
179 covered that guanidine hydrochloride rescues septin function in cdc10 mutants by promoting assembly o
182 le structurally a cytoskeleton-like element, septins function predominantly as spatial regulators of
185 ng protein Septin 9 (SEPT9), a member of the septin gene family, has been proposed to have oncogenic
188 we analyzed the position and orientation of septin-GFP molecules incorporated in septin bundles in g
194 pansion in vivo and thus show that targeting septins has strong potential to moderate detrimental bys
197 th anniversary perspective, we highlight how septins have conserved and adapted their roles as effect
199 ay produces the two species of budding yeast septin hetero-octamers: Cdc11/Shs1-Cdc12-Cdc3-Cdc10-Cdc1
200 interface") cause thermoinstability of yeast septin hetero-oligomer assembly, and human disease.
201 G interface mutants, operates during de novo septin hetero-oligomer assembly, and requires specific c
202 ently, even for the best characterized human septin heterocomplex (SEPT2/SEPT6/SEPT7), the role of C-
203 mics with SEPT2/6/7, the minimal subunits of septin heteromers, shows that SEPT2/6/7 has a biphasic c
205 t [16, 17], specifically associates with the septin hourglass during the cell cycle and controls hour
206 Hsl1 reportedly interacts with particular septins; however, the precise molecular determinants in
207 of macropinosomes/endosomes is abrogated by septin immunodepletion and function-blocking antibodies
208 re required for the retention of anillin and septin in the anterior pole, which are cytokinesis prote
211 ether, our data identify a critical role for septins in regulating the release of lytic granule conte
212 ing antibodies and is induced by recombinant septins in the absence of cytosol and polymerized actin.
213 iews emerging evidence implicating different septins in the regulation of host-pathogen interactions,
221 follow the binding to septin filaments of a septin-interacting protein, the type II myosin-binding p
223 complex that contains both meiosis-specific septins is a linear Spr28-Spr3-Cdc3-Cdc10-Cdc10-Cdc3-Spr
224 that encompasses the GTP-binding pocket of a septin (its "G interface") cause thermoinstability of ye
228 ion of the LEP protein Ssp1 perturbs mitotic septin localization and function, suggesting a functiona
231 Our findings reveal a mechanism underlying septin-mediated infection structure formation in fungi a
233 is applied as an enormous invasive force by septin-mediated reorganization of the cytoskeleton and a
236 rt that directed PSM extension fails in many septin-mutant cells, and, for those that do succeed, wal
240 cer cell motility that coordinates actin and septin networks and describes a unique role for SEPT9 in
242 These data show that curvature sensing by septins operates at much smaller length scales than the
243 ke kinase Elm1, which has been implicated in septin organization [14], cell morphogenesis [15], and m
247 nce was important for the recruitment of the septin Peanut and distribution of Diaphanous and F-actin
251 oduction and proper assembly of Sep4, a core septin protein and virulence determinant, to initiate in
255 s impaired conjugate formation, depletion of septin proteins had no impact on conjugate formation, ly
258 at features of the plasma membrane influence septin recruitment and alternatively, how septins influe
261 hrough interaction with STIM proteins, while septins regulate the number of ER-PM junctions and enhan
265 We propose that Rho1 and Pkc1 coordinate septin ring assembly with membrane and cell wall remodel
267 Here we show that recruitment of Hsl7 to the septin ring depends on a combination of two septin-bindi
278 4,5)-bisphosphate (PI(4,5)P2)-levels, myelin septins (SEPT2/SEPT4/SEPT7/SEPT8) and the PI(4,5)P2-adap
286 circumstances, the polar cap travels toward septin structures and away from sites of exocytosis, res
288 g meiosis Spr3 and Spr28 replace the mitotic septin subunits Cdc12 and Cdc11 (and Shs1), respectively
290 with the organization and behavior of yeast septins suggesting that their properties are more conser
291 ve been characterized as having misregulated septins, suggesting that their functions are relevant to
292 Cells choose from a variety of available septins to assemble distinct hetero-oligomers, but the u
293 nformational change, have been repurposed in septins to play a fundamental role in molecular recognit
294 ce studies revealed high-affinity binding of septins to the microtubule plus-end tracking protein EB1
295 s to specific defects in mRNA, ribosome, and septin transport without affecting general functions of
296 not interact with septin-2, indicating that septins undergo reorganization during each exocytosis cy
297 bud emergence, Hsl7 is not recruited to the septins until after bud emergence, suggesting that septi
298 onstrate that expression of non-SUMOylatable septin variants from the SEPT6 and SEPT7 groups leads to
300 contrast, cell division was not dependent on septins when cell-cell contacts, such as those with anti