---
_id: '7776'
abstract:
- lang: eng
text: We present an analysis of finite-size effects in jammed packings of N soft,
frictionless spheres at zero temperature. There is a 1/N correction to the discrete
jump in the contact number at the transition so that jammed packings exist only
above isostaticity. As a result, the canonical power-law scalings of the contact
number and elastic moduli break down at low pressure. These quantities exhibit
scaling collapse with a nontrivial scaling function, demonstrating that the jamming
transition can be considered a phase transition. Scaling is achieved as a function
of N in both two and three dimensions, indicating an upper critical dimension
of 2.
article_number: '095704'
article_processing_charge: No
article_type: original
author:
- first_name: Carl Peter
full_name: Goodrich, Carl Peter
id: EB352CD2-F68A-11E9-89C5-A432E6697425
last_name: Goodrich
orcid: 0000-0002-1307-5074
- first_name: Andrea J.
full_name: Liu, Andrea J.
last_name: Liu
- first_name: Sidney R.
full_name: Nagel, Sidney R.
last_name: Nagel
citation:
ama: Goodrich CP, Liu AJ, Nagel SR. Finite-size scaling at the jamming transition.
Physical Review Letters. 2012;109(9). doi:10.1103/physrevlett.109.095704
apa: Goodrich, C. P., Liu, A. J., & Nagel, S. R. (2012). Finite-size scaling
at the jamming transition. Physical Review Letters. American Physical Society.
https://doi.org/10.1103/physrevlett.109.095704
chicago: Goodrich, Carl Peter, Andrea J. Liu, and Sidney R. Nagel. “Finite-Size
Scaling at the Jamming Transition.” Physical Review Letters. American Physical
Society, 2012. https://doi.org/10.1103/physrevlett.109.095704.
ieee: C. P. Goodrich, A. J. Liu, and S. R. Nagel, “Finite-size scaling at the jamming
transition,” Physical Review Letters, vol. 109, no. 9. American Physical
Society, 2012.
ista: Goodrich CP, Liu AJ, Nagel SR. 2012. Finite-size scaling at the jamming transition.
Physical Review Letters. 109(9), 095704.
mla: Goodrich, Carl Peter, et al. “Finite-Size Scaling at the Jamming Transition.”
Physical Review Letters, vol. 109, no. 9, 095704, American Physical Society,
2012, doi:10.1103/physrevlett.109.095704.
short: C.P. Goodrich, A.J. Liu, S.R. Nagel, Physical Review Letters 109 (2012).
date_created: 2020-04-30T11:44:12Z
date_published: 2012-08-27T00:00:00Z
date_updated: 2021-01-12T08:15:27Z
day: '27'
doi: 10.1103/physrevlett.109.095704
extern: '1'
intvolume: ' 109'
issue: '9'
language:
- iso: eng
month: '08'
oa_version: None
publication: Physical Review Letters
publication_identifier:
issn:
- 0031-9007
- 1079-7114
publication_status: published
publisher: American Physical Society
quality_controlled: '1'
status: public
title: Finite-size scaling at the jamming transition
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 109
year: '2012'
...
---
_id: '801'
abstract:
- lang: eng
text: Fungal cell walls frequently contain a polymer of mannose and galactose called
galactomannan. In the pathogenic filamentous fungus Aspergillus fumigatus, this
polysaccharide is made of a linear mannan backbone with side chains of galactofuran
and is anchored to the plasma membrane via a glycosylphosphatidylinositol or is
covalently linked to the cell wall. To date, the biosynthesis and significance
of this polysaccharide are unknown. The present data demonstrate that deletion
of the Golgi UDP-galactofuranose transporter GlfB or the GDP-mannose transporter
GmtA leads to the absence of galactofuran or galactomannan, respectively. This
indicates that the biosynthesis of galactomannan probably occurs in the lumen
of the Golgi apparatus and thus contrasts with the biosynthesis of other fungal
cell wall polysaccharides studied to date that takes place at the plasma membrane.
Transglycosylation of galactomannan from the membrane to the cell wall is hypothesized
because both the cell wall-bound and membrane-bound polysaccharide forms are affected
in the generated mutants. Considering the severe growth defect of the A. fumigatus
GmtA-deficient mutant, proving this paradigm might provide new targets for antifungal
therapy.
acknowledgement: This work was supported by the Deutsche Forschungsgemeinschaft.
article_processing_charge: No
article_type: original
author:
- first_name: Jakob
full_name: Engel, Jakob
last_name: Engel
- first_name: Philipp S
full_name: Schmalhorst, Philipp S
id: 309D50DA-F248-11E8-B48F-1D18A9856A87
last_name: Schmalhorst
orcid: 0000-0002-5795-0133
- first_name: Françoise
full_name: Routier, Françoise
last_name: Routier
citation:
ama: Engel J, Schmalhorst PS, Routier F. Biosynthesis of the fungal cell wall polysaccharide
galactomannan requires intraluminal GDP-mannose. Journal of Biological Chemistry.
2012;287(53):44418-44424. doi:10.1074/jbc.M112.398321
apa: Engel, J., Schmalhorst, P. S., & Routier, F. (2012). Biosynthesis of the
fungal cell wall polysaccharide galactomannan requires intraluminal GDP-mannose.
Journal of Biological Chemistry. American Society for Biochemistry and
Molecular Biology. https://doi.org/10.1074/jbc.M112.398321
chicago: Engel, Jakob, Philipp S Schmalhorst, and Françoise Routier. “Biosynthesis
of the Fungal Cell Wall Polysaccharide Galactomannan Requires Intraluminal GDP-Mannose.”
Journal of Biological Chemistry. American Society for Biochemistry and
Molecular Biology, 2012. https://doi.org/10.1074/jbc.M112.398321.
ieee: J. Engel, P. S. Schmalhorst, and F. Routier, “Biosynthesis of the fungal cell
wall polysaccharide galactomannan requires intraluminal GDP-mannose,” Journal
of Biological Chemistry, vol. 287, no. 53. American Society for Biochemistry
and Molecular Biology, pp. 44418–44424, 2012.
ista: Engel J, Schmalhorst PS, Routier F. 2012. Biosynthesis of the fungal cell
wall polysaccharide galactomannan requires intraluminal GDP-mannose. Journal of
Biological Chemistry. 287(53), 44418–44424.
mla: Engel, Jakob, et al. “Biosynthesis of the Fungal Cell Wall Polysaccharide Galactomannan
Requires Intraluminal GDP-Mannose.” Journal of Biological Chemistry, vol.
287, no. 53, American Society for Biochemistry and Molecular Biology, 2012, pp.
44418–24, doi:10.1074/jbc.M112.398321.
short: J. Engel, P.S. Schmalhorst, F. Routier, Journal of Biological Chemistry 287
(2012) 44418–44424.
date_created: 2018-12-11T11:48:34Z
date_published: 2012-12-28T00:00:00Z
date_updated: 2022-03-21T07:57:14Z
day: '28'
doi: 10.1074/jbc.M112.398321
extern: '1'
external_id:
pmid:
- '23139423'
intvolume: ' 287'
issue: '53'
language:
- iso: eng
month: '12'
oa_version: None
page: 44418 - 44424
pmid: 1
publication: Journal of Biological Chemistry
publication_status: published
publisher: American Society for Biochemistry and Molecular Biology
publist_id: '6852'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Biosynthesis of the fungal cell wall polysaccharide galactomannan requires
intraluminal GDP-mannose
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 287
year: '2012'
...
---
_id: '8024'
abstract:
- lang: eng
text: In dynamical models of cortical networks, the recurrent connectivity can amplify
the input given to the network in two distinct ways. One is induced by the presence
of near-critical eigenvalues in the connectivity matrix W, producing large but
slow activity fluctuations along the corresponding eigenvectors (dynamical slowing).
The other relies on W not being normal, which allows the network activity to make
large but fast excursions along specific directions. Here we investigate the trade-off
between non-normal amplification and dynamical slowing in the spontaneous activity
of large random neuronal networks composed of excitatory and inhibitory neurons.
We use a Schur decomposition of W to separate the two amplification mechanisms.
Assuming linear stochastic dynamics, we derive an exact expression for the expected
amount of purely non-normal amplification. We find that amplification is very
limited if dynamical slowing must be kept weak. We conclude that, to achieve strong
transient amplification with little slowing, the connectivity must be structured.
We show that unidirectional connections between neurons of the same type together
with reciprocal connections between neurons of different types, allow for amplification
already in the fast dynamical regime. Finally, our results also shed light on
the differences between balanced networks in which inhibition exactly cancels
excitation and those where inhibition dominates.
article_number: '011909'
article_processing_charge: No
article_type: original
author:
- first_name: Guillaume
full_name: Hennequin, Guillaume
last_name: Hennequin
- first_name: Tim P
full_name: Vogels, Tim P
id: CB6FF8D2-008F-11EA-8E08-2637E6697425
last_name: Vogels
orcid: 0000-0003-3295-6181
- first_name: Wulfram
full_name: Gerstner, Wulfram
last_name: Gerstner
citation:
ama: Hennequin G, Vogels TP, Gerstner W. Non-normal amplification in random balanced
neuronal networks. Physical Review E. 2012;86(1). doi:10.1103/physreve.86.011909
apa: Hennequin, G., Vogels, T. P., & Gerstner, W. (2012). Non-normal amplification
in random balanced neuronal networks. Physical Review E. American Physical
Society. https://doi.org/10.1103/physreve.86.011909
chicago: Hennequin, Guillaume, Tim P Vogels, and Wulfram Gerstner. “Non-Normal Amplification
in Random Balanced Neuronal Networks.” Physical Review E. American Physical
Society, 2012. https://doi.org/10.1103/physreve.86.011909.
ieee: G. Hennequin, T. P. Vogels, and W. Gerstner, “Non-normal amplification in
random balanced neuronal networks,” Physical Review E, vol. 86, no. 1.
American Physical Society, 2012.
ista: Hennequin G, Vogels TP, Gerstner W. 2012. Non-normal amplification in random
balanced neuronal networks. Physical Review E. 86(1), 011909.
mla: Hennequin, Guillaume, et al. “Non-Normal Amplification in Random Balanced Neuronal
Networks.” Physical Review E, vol. 86, no. 1, 011909, American Physical
Society, 2012, doi:10.1103/physreve.86.011909.
short: G. Hennequin, T.P. Vogels, W. Gerstner, Physical Review E 86 (2012).
date_created: 2020-06-25T13:09:06Z
date_published: 2012-06-11T00:00:00Z
date_updated: 2021-01-12T08:16:35Z
day: '11'
doi: 10.1103/physreve.86.011909
extern: '1'
external_id:
pmid:
- '23005454'
intvolume: ' 86'
issue: '1'
language:
- iso: eng
month: '06'
oa_version: None
pmid: 1
publication: Physical Review E
publication_identifier:
eisbn:
- 1550-2376
issn:
- 1539-3755
publication_status: published
publisher: American Physical Society
quality_controlled: '1'
status: public
title: Non-normal amplification in random balanced neuronal networks
type: journal_article
user_id: D865714E-FA4E-11E9-B85B-F5C5E5697425
volume: 86
year: '2012'
...
---
_id: '808'
abstract:
- lang: eng
text: Using correlated live-cell imaging and electron tomography we found that actin
branch junctions in protruding and treadmilling lamellipodia are not concentrated
at the front as previously supposed, but link actin filament subsets in which
there is a continuum of distances from a junction to the filament plus ends, for
up to at least 1 mm. When branch sites were observed closely spaced on the same
filament their separation was commonly a multiple of the actin helical repeat
of 36 nm. Image averaging of branch junctions in the tomograms yielded a model
for the in vivo branch at 2.9 nm resolution, which was comparable with that derived
for the in vitro actin- Arp2/3 complex. Lamellipodium initiation was monitored
in an intracellular wound-healing model and was found to involve branching from
the sides of actin filaments oriented parallel to the plasmalemma. Many filament
plus ends, presumably capped, terminated behind the lamellipodium tip and localized
on the dorsal and ventral surfaces of the actin network. These findings reveal
how branching events initiate and maintain a network of actin filaments of variable
length, and provide the first structural model of the branch junction in vivo.
A possible role of filament capping in generating the lamellipodium leaflet is
discussed and a mathematical model of protrusion is also presented.
acknowledgement: This work was supported by the Austrian Science Fund [projects FWF
I516-B09 and FWF P21292-B09 to J.V.S.]; the Vienna Science and Technology Fund [WWTF-grant
numbers MA 09-004 to J.V.S. and C.S], ZIT - The Technology Agency of the City of
Vienna [VSOE, CMCN to J.V.S. and G.P.R.]; the Deutsche Forschungsgemeinschaft [grant
number RO 2414/1-2 to K.R.]; the Daiko research foundation [grant number 9134 to
A.N.]; and a Grant-in-Aid for Scientific Research [S, grant number 20227008 to Y.M.]
and a Grant-in-Aid for Young Scientists [B, grant number 22770145 to A.N.] (B) from
The Ministry of Education, Culture, Sports, Science and Technology of the Japanese
Government. Deposited in PMC for immediate release. We thank Tibor Kulcsar for assistance
with graphics.
author:
- first_name: Marlene
full_name: Vinzenz, Marlene
last_name: Vinzenz
- first_name: Maria
full_name: Nemethova, Maria
id: 34E27F1C-F248-11E8-B48F-1D18A9856A87
last_name: Nemethova
- first_name: Florian
full_name: Schur, Florian
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
- first_name: Jan
full_name: Mueller, Jan
last_name: Mueller
- first_name: Akihiro
full_name: Narita, Akihiro
last_name: Narita
- first_name: Edit
full_name: Urban, Edit
last_name: Urban
- first_name: Christoph
full_name: Winkler, Christoph
last_name: Winkler
- first_name: Christian
full_name: Schmeiser, Christian
last_name: Schmeiser
- first_name: Stefan
full_name: Koestler, Stefan
last_name: Koestler
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Guenter
full_name: Resch, Guenter
last_name: Resch
- first_name: Yuichiro
full_name: Maéda, Yuichiro
last_name: Maéda
- first_name: John
full_name: Small, John
last_name: Small
citation:
ama: Vinzenz M, Nemethova M, Schur FK, et al. Actin branching in the initiation
and maintenance of lamellipodia. Journal of Cell Science. 2012;125(11):2775-2785.
doi:10.1242/jcs.107623
apa: Vinzenz, M., Nemethova, M., Schur, F. K., Mueller, J., Narita, A., Urban, E.,
… Small, J. (2012). Actin branching in the initiation and maintenance of lamellipodia.
Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.107623
chicago: Vinzenz, Marlene, Maria Nemethova, Florian KM Schur, Jan Mueller, Akihiro
Narita, Edit Urban, Christoph Winkler, et al. “Actin Branching in the Initiation
and Maintenance of Lamellipodia.” Journal of Cell Science. Company of Biologists,
2012. https://doi.org/10.1242/jcs.107623.
ieee: M. Vinzenz et al., “Actin branching in the initiation and maintenance
of lamellipodia,” Journal of Cell Science, vol. 125, no. 11. Company of
Biologists, pp. 2775–2785, 2012.
ista: Vinzenz M, Nemethova M, Schur FK, Mueller J, Narita A, Urban E, Winkler C,
Schmeiser C, Koestler S, Rottner K, Resch G, Maéda Y, Small J. 2012. Actin branching
in the initiation and maintenance of lamellipodia. Journal of Cell Science. 125(11),
2775–2785.
mla: Vinzenz, Marlene, et al. “Actin Branching in the Initiation and Maintenance
of Lamellipodia.” Journal of Cell Science, vol. 125, no. 11, Company of
Biologists, 2012, pp. 2775–85, doi:10.1242/jcs.107623.
short: M. Vinzenz, M. Nemethova, F.K. Schur, J. Mueller, A. Narita, E. Urban, C.
Winkler, C. Schmeiser, S. Koestler, K. Rottner, G. Resch, Y. Maéda, J. Small,
Journal of Cell Science 125 (2012) 2775–2785.
date_created: 2018-12-11T11:48:37Z
date_published: 2012-06-01T00:00:00Z
date_updated: 2021-01-12T08:16:47Z
day: '01'
ddc:
- '570'
doi: 10.1242/jcs.107623
extern: '1'
file:
- access_level: open_access
checksum: 2f59e15cc3a85bb500a9887cef2aab67
content_type: application/pdf
creator: kschuh
date_created: 2019-02-12T08:54:51Z
date_updated: 2020-07-14T12:48:09Z
file_id: '5956'
file_name: 2012_Biologists_Vinzenz.pdf
file_size: 3326073
relation: main_file
file_date_updated: 2020-07-14T12:48:09Z
has_accepted_license: '1'
intvolume: ' 125'
issue: '11'
language:
- iso: eng
month: '06'
oa: 1
oa_version: None
page: 2775 - 2785
publication: Journal of Cell Science
publication_status: published
publisher: Company of Biologists
publist_id: '6842'
quality_controlled: '1'
status: public
title: Actin branching in the initiation and maintenance of lamellipodia
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 125
year: '2012'
...
---
_id: '8246'
abstract:
- lang: eng
text: The Staphylococcus aureus cell wall stress stimulon (CWSS) is activated by
cell envelope-targeting antibiotics or depletion of essential cell wall biosynthesis
enzymes. The functionally uncharacterized S. aureus LytR-CpsA-Psr (LCP) proteins,
MsrR, SA0908 and SA2103, all belong to the CWSS. Although not essential, deletion
of all three LCP proteins severely impairs cell division. We show here that VraSR-dependent
CWSS expression was up to 250-fold higher in single, double and triple LCP mutants
than in wild type S. aureus in the absence of external stress. The LCP triple
mutant was virtually depleted of wall teichoic acids (WTA), which could be restored
to different degrees by any of the single LCP proteins. Subinhibitory concentrations
of tunicamycin, which inhibits the first WTA synthesis enzyme TarO (TagO), could
partially complement the severe growth defect of the LCP triple mutant. Both of
the latter findings support a role for S. aureus LCP proteins in late WTA synthesis,
as in Bacillus subtilis where LCP proteins were recently proposed to transfer
WTA from lipid carriers to the cell wall peptidoglycan. Intrinsic activation of
the CWSS upon LCP deletion and the fact that LCP proteins were essential for WTA-loading
of the cell wall, highlight their important role(s) in S. aureus cell envelope
biogenesis.
article_processing_charge: No
article_type: original
author:
- first_name: Vanina
full_name: Dengler, Vanina
last_name: Dengler
- first_name: Patricia Stutzmann
full_name: Meier, Patricia Stutzmann
last_name: Meier
- first_name: Ronald
full_name: Heusser, Ronald
last_name: Heusser
- first_name: Peter
full_name: Kupferschmied, Peter
last_name: Kupferschmied
- first_name: Judit
full_name: Fazekas, Judit
id: 36432834-F248-11E8-B48F-1D18A9856A87
last_name: Fazekas
orcid: 0000-0002-8777-3502
- first_name: Sarah
full_name: Friebe, Sarah
last_name: Friebe
- first_name: Sibylle Burger
full_name: Staufer, Sibylle Burger
last_name: Staufer
- first_name: Paul A.
full_name: Majcherczyk, Paul A.
last_name: Majcherczyk
- first_name: Philippe
full_name: Moreillon, Philippe
last_name: Moreillon
- first_name: Brigitte
full_name: Berger-Bächi, Brigitte
last_name: Berger-Bächi
- first_name: Nadine
full_name: McCallum, Nadine
last_name: McCallum
citation:
ama: Dengler V, Meier PS, Heusser R, et al. Deletion of hypothetical wall teichoic
acid ligases in Staphylococcus aureus activates the cell wall stress response.
FEMS Microbiology Letters. 2012;333(2):109-120. doi:10.1111/j.1574-6968.2012.02603.x
apa: Dengler, V., Meier, P. S., Heusser, R., Kupferschmied, P., Singer, J., Friebe,
S., … McCallum, N. (2012). Deletion of hypothetical wall teichoic acid ligases
in Staphylococcus aureus activates the cell wall stress response. FEMS Microbiology
Letters. Oxford University Press. https://doi.org/10.1111/j.1574-6968.2012.02603.x
chicago: Dengler, Vanina, Patricia Stutzmann Meier, Ronald Heusser, Peter Kupferschmied,
Judit Singer, Sarah Friebe, Sibylle Burger Staufer, et al. “Deletion of Hypothetical
Wall Teichoic Acid Ligases in Staphylococcus Aureus Activates the Cell Wall Stress
Response.” FEMS Microbiology Letters. Oxford University Press, 2012. https://doi.org/10.1111/j.1574-6968.2012.02603.x.
ieee: V. Dengler et al., “Deletion of hypothetical wall teichoic acid ligases
in Staphylococcus aureus activates the cell wall stress response,” FEMS Microbiology
Letters, vol. 333, no. 2. Oxford University Press, pp. 109–120, 2012.
ista: Dengler V, Meier PS, Heusser R, Kupferschmied P, Singer J, Friebe S, Staufer
SB, Majcherczyk PA, Moreillon P, Berger-Bächi B, McCallum N. 2012. Deletion of
hypothetical wall teichoic acid ligases in Staphylococcus aureus activates the
cell wall stress response. FEMS Microbiology Letters. 333(2), 109–120.
mla: Dengler, Vanina, et al. “Deletion of Hypothetical Wall Teichoic Acid Ligases
in Staphylococcus Aureus Activates the Cell Wall Stress Response.” FEMS Microbiology
Letters, vol. 333, no. 2, Oxford University Press, 2012, pp. 109–20, doi:10.1111/j.1574-6968.2012.02603.x.
short: V. Dengler, P.S. Meier, R. Heusser, P. Kupferschmied, J. Singer, S. Friebe,
S.B. Staufer, P.A. Majcherczyk, P. Moreillon, B. Berger-Bächi, N. McCallum, FEMS
Microbiology Letters 333 (2012) 109–120.
date_created: 2020-08-10T11:54:47Z
date_published: 2012-08-01T00:00:00Z
date_updated: 2021-01-12T08:17:43Z
day: '01'
doi: 10.1111/j.1574-6968.2012.02603.x
extern: '1'
external_id:
pmid:
- '22640011'
intvolume: ' 333'
issue: '2'
language:
- iso: eng
month: '08'
oa_version: None
page: 109-120
pmid: 1
publication: FEMS Microbiology Letters
publication_identifier:
issn:
- 0378-1097
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
status: public
title: Deletion of hypothetical wall teichoic acid ligases in Staphylococcus aureus
activates the cell wall stress response
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 333
year: '2012'
...