---
_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
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
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'
...
---
_id: '826'
abstract:
- lang: eng
text: Plants exhibit a unique developmental flexibility to ever-changing environmental
conditions. To achieve their profound adaptability, plants are able to maintain
permanent stem cell populations and form new organs during the entire plant life
cycle. Signaling substances, called plant hormones, such as auxin, cytokinin,
abscisic acid, brassinosteroid, ethylene, gibberellin, jasmonic acid, and strigolactone,
govern and coordinate these developmental processes. Physiological and genetic
studies have dissected the molecular components of signal perception and transduction
of the individual hormonal pathways. However, over recent years it has become
evident that hormones do not act only in a linear pathway. Hormonal pathways are
interconnected by a complex network of interactions and feedback circuits that
determines the final outcome of the individual hormone actions. This raises questions
about the molecular mechanisms underlying hormonal cross talk and about how these
hormonal networks are established, maintained, and modulated throughout plant
development.
acknowledgement: We would like to thank Annick Bleys for help in preparing the manuscript.
This work was supported by the European Research Council with a Starting Independent
Research grant (ERC-2007-Stg-207362-HCPO) and the project CZ.1.07/2.3.00/20.0043
(to the Central European Institute of Technology, CEITEC) to E.B. M.V. is a postdoctoral
fellow of the Research Foundation Flanders. We apologize that, because of space
restrictions, the scientific contributions of only a limited number of original
articles could be cited and discussed.
author:
- first_name: Marleen
full_name: Vanstraelen, Marleen
last_name: Vanstraelen
- first_name: Eva
full_name: Eva Benková
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
citation:
ama: Vanstraelen M, Benková E. Hormonal interactions in the regulation of plant
development. Annual Review of Cell and Developmental Biology. 2012;28:463-487.
doi:10.1146/annurev-cellbio-101011-155741
apa: Vanstraelen, M., & Benková, E. (2012). Hormonal interactions in the regulation
of plant development. Annual Review of Cell and Developmental Biology.
Annual Reviews. https://doi.org/10.1146/annurev-cellbio-101011-155741
chicago: Vanstraelen, Marleen, and Eva Benková. “Hormonal Interactions in the Regulation
of Plant Development.” Annual Review of Cell and Developmental Biology.
Annual Reviews, 2012. https://doi.org/10.1146/annurev-cellbio-101011-155741.
ieee: M. Vanstraelen and E. Benková, “Hormonal interactions in the regulation of
plant development,” Annual Review of Cell and Developmental Biology, vol.
28. Annual Reviews, pp. 463–487, 2012.
ista: Vanstraelen M, Benková E. 2012. Hormonal interactions in the regulation of
plant development. Annual Review of Cell and Developmental Biology. 28, 463–487.
mla: Vanstraelen, Marleen, and Eva Benková. “Hormonal Interactions in the Regulation
of Plant Development.” Annual Review of Cell and Developmental Biology,
vol. 28, Annual Reviews, 2012, pp. 463–87, doi:10.1146/annurev-cellbio-101011-155741.
short: M. Vanstraelen, E. Benková, Annual Review of Cell and Developmental Biology
28 (2012) 463–487.
date_created: 2018-12-11T11:48:43Z
date_published: 2012-11-01T00:00:00Z
date_updated: 2021-01-12T08:17:46Z
day: '01'
doi: 10.1146/annurev-cellbio-101011-155741
extern: 1
intvolume: ' 28'
month: '11'
page: 463 - 487
publication: Annual Review of Cell and Developmental Biology
publication_status: published
publisher: Annual Reviews
publist_id: '6822'
quality_controlled: 0
status: public
title: Hormonal interactions in the regulation of plant development
type: journal_article
volume: 28
year: '2012'
...
---
_id: '829'
abstract:
- lang: eng
text: The architecture of a plant's root system, established postembryonically,
results from both coordinated root growth and lateral root branching. The plant
hormones auxin and cytokinin are central endogenous signaling molecules that regulate
lateral root organogenesis positively and negatively, respectively. Tight control
and mutual balance of their antagonistic activities are particularly important
during the early phases of lateral root organogenesis to ensure continuous lateral
root initiation (LRI) and proper development of lateral root primordia (LRP).
Here, we show that the early phases of lateral root organogenesis, including priming
and initiation, take place in root zones with a repressed cytokinin response.
Accordingly, ectopic overproduction of cytokinin in the root basal meristem most
efficiently inhibits LRI. Enhanced cytokinin responses in pericycle cells between
existing LRP might restrict LRI near existing LRP and, when compromised, ectopic
LRI occurs. Furthermore, our results demonstrate that young LRP are more sensitive
to perturbations in the cytokinin activity than are developmentally more advanced
primordia. We hypothesize that the effect of cytokinin on the development of primordia
possibly depends on the robustness and stability of the auxin gradient.
acknowledgement: We thank Jen Sheen, Dolf Weijers, Tatsuo Kakimoto, Stephen Depuydt,
and Laurent Laplaze for sharing published material, Jiri Friml for discussions,
and Martine De Cock and Annick Bleys for help in preparing the manuscript. This
work was supported by a Starting Independent Research grant from the European Research
Council (ERC-2007-Stg-207362-HCPO) and the project CZ.1.07/2.3.00/20.0043 to the
Central European Institute of Technology to E.B. and grants from the Ministry of
Education, Youth, and Sports of the Czech Republic (MSM 6198959216) and the Centre
of the Region Haná for Biotechnological and Agricultural Research (ED0007/01/01)
to P.T.
author:
- first_name: Agnieszka
full_name: Bielach, Agnieszka
last_name: Bielach
- first_name: Katerina
full_name: Podlesakova, Katerina
last_name: Podlesakova
- first_name: Peter
full_name: Peter Marhavy
id: 3F45B078-F248-11E8-B48F-1D18A9856A87
last_name: Marhavy
orcid: 0000-0001-5227-5741
- first_name: Jérôme
full_name: Duclercq, Jérôme
last_name: Duclercq
- first_name: Candela
full_name: Candela Cuesta
id: 33A3C818-F248-11E8-B48F-1D18A9856A87
last_name: Cuesta
orcid: 0000-0003-1923-2410
- first_name: Bruno
full_name: Muller, Bruno
last_name: Muller
- first_name: Wim
full_name: Grunewald, Wim
last_name: Grunewald
- first_name: Petr
full_name: Tarkowski, Petr
last_name: Tarkowski
- first_name: Eva
full_name: Eva Benková
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
citation:
ama: Bielach A, Podlesakova K, Marhavý P, et al. Spatiotemporal regulation of lateral
root organogenesis in Arabidopsis by cytokinin. The Plant Cell. 2012;24(10):3967-3981.
doi:10.1105/tpc.112.103044
apa: Bielach, A., Podlesakova, K., Marhavý, P., Duclercq, J., Cuesta, C., Muller,
B., … Benková, E. (2012). Spatiotemporal regulation of lateral root organogenesis
in Arabidopsis by cytokinin. The Plant Cell. American Society of Plant
Biologists. https://doi.org/10.1105/tpc.112.103044
chicago: Bielach, Agnieszka, Katerina Podlesakova, Peter Marhavý, Jérôme Duclercq,
Candela Cuesta, Bruno Muller, Wim Grunewald, Petr Tarkowski, and Eva Benková.
“Spatiotemporal Regulation of Lateral Root Organogenesis in Arabidopsis by Cytokinin.”
The Plant Cell. American Society of Plant Biologists, 2012. https://doi.org/10.1105/tpc.112.103044.
ieee: A. Bielach et al., “Spatiotemporal regulation of lateral root organogenesis
in Arabidopsis by cytokinin,” The Plant Cell, vol. 24, no. 10. American
Society of Plant Biologists, pp. 3967–3981, 2012.
ista: Bielach A, Podlesakova K, Marhavý P, Duclercq J, Cuesta C, Muller B, Grunewald
W, Tarkowski P, Benková E. 2012. Spatiotemporal regulation of lateral root organogenesis
in Arabidopsis by cytokinin. The Plant Cell. 24(10), 3967–3981.
mla: Bielach, Agnieszka, et al. “Spatiotemporal Regulation of Lateral Root Organogenesis
in Arabidopsis by Cytokinin.” The Plant Cell, vol. 24, no. 10, American
Society of Plant Biologists, 2012, pp. 3967–81, doi:10.1105/tpc.112.103044.
short: A. Bielach, K. Podlesakova, P. Marhavý, J. Duclercq, C. Cuesta, B. Muller,
W. Grunewald, P. Tarkowski, E. Benková, The Plant Cell 24 (2012) 3967–3981.
date_created: 2018-12-11T11:48:43Z
date_published: 2012-10-01T00:00:00Z
date_updated: 2021-01-12T08:17:55Z
day: '01'
doi: 10.1105/tpc.112.103044
extern: 1
intvolume: ' 24'
issue: '10'
month: '10'
page: 3967 - 3981
publication: The Plant Cell
publication_status: published
publisher: American Society of Plant Biologists
publist_id: '6819'
quality_controlled: 0
status: public
title: Spatiotemporal regulation of lateral root organogenesis in Arabidopsis by cytokinin
type: journal_article
volume: 24
year: '2012'
...
---
_id: '846'
abstract:
- lang: eng
text: Whether or not evolutionary change is inherently irreversible remains a controversial
topic. Some examples of evolutionary irreversibility are known; however, this
question has not been comprehensively addressed at the molecular level. Here,
we use data from 221 human genes with known pathogenic mutations to estimate the
rate of irreversibility in protein evolution. For these genes, we reconstruct
ancestral amino acid sequences along the mammalian phylogeny and identify ancestral
amino acid states that match known pathogenic mutations. Such cases represent
inherent evolutionary irreversibility because, at the present moment, reversals
to these ancestral amino acid states are impossible for the human lineage. We
estimate that approximately 10% of all amino acid substitutions along the mammalian
phylogeny are irreversible, such that a return to the ancestral amino acid state
would lead to a pathogenic phenotype. For a subset of 51 genes with high rates
of irreversibility, as much as 40% of all amino acid evolution was estimated to
be irreversible. Because pathogenic phenotypes do not resemble ancestral phenotypes,
the molecular nature of the high rate of irreversibility in proteins is best explained
by evolution with a high prevalence of compensatory, epistatic interactions between
amino acid sites. Under such mode of protein evolution, once an amino acid substitution
is fixed, the probability of its reversal declines as the protein sequence accumulates
changes that affect the phenotypic manifestation of the ancestral state. The prevalence
of epistasis in evolution indicates that the observed high rate of irreversibility
in protein evolution is an inherent property of protein structure and function.
acknowledgement: This work was supported by Plan Nacional grant BFU2009-09271 from
the Spanish Ministry of Science and Innovation and by FPU (Formación del Profesorado
Universitario) program grant AP2008-01888 from the Spanish Ministry of Education
to O.S. F.A.K. is a European Molecular Biology Organization Young Investigator and
Howard Hughes Medical Institute International Early Career Scientist.
author:
- first_name: Onuralp
full_name: Soylemez, Onuralp
last_name: Soylemez
- first_name: Fyodor
full_name: Fyodor Kondrashov
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
citation:
ama: Soylemez O, Kondrashov F. Estimating the rate of irreversibility in protein
evolution. Genome Biology and Evolution. 2012;4(12):1213-1222. doi:10.1093/gbe/evs096
apa: Soylemez, O., & Kondrashov, F. (2012). Estimating the rate of irreversibility
in protein evolution. Genome Biology and Evolution. Oxford University Press.
https://doi.org/10.1093/gbe/evs096
chicago: Soylemez, Onuralp, and Fyodor Kondrashov. “Estimating the Rate of Irreversibility
in Protein Evolution.” Genome Biology and Evolution. Oxford University
Press, 2012. https://doi.org/10.1093/gbe/evs096.
ieee: O. Soylemez and F. Kondrashov, “Estimating the rate of irreversibility in
protein evolution,” Genome Biology and Evolution, vol. 4, no. 12. Oxford
University Press, pp. 1213–1222, 2012.
ista: Soylemez O, Kondrashov F. 2012. Estimating the rate of irreversibility in
protein evolution. Genome Biology and Evolution. 4(12), 1213–1222.
mla: Soylemez, Onuralp, and Fyodor Kondrashov. “Estimating the Rate of Irreversibility
in Protein Evolution.” Genome Biology and Evolution, vol. 4, no. 12, Oxford
University Press, 2012, pp. 1213–22, doi:10.1093/gbe/evs096.
short: O. Soylemez, F. Kondrashov, Genome Biology and Evolution 4 (2012) 1213–1222.
date_created: 2018-12-11T11:48:49Z
date_published: 2012-01-01T00:00:00Z
date_updated: 2021-01-12T08:19:25Z
day: '01'
doi: 10.1093/gbe/evs096
extern: 1
intvolume: ' 4'
issue: '12'
license: https://creativecommons.org/licenses/by-nc/4.0/
month: '01'
page: 1213 - 1222
publication: Genome Biology and Evolution
publication_status: published
publisher: Oxford University Press
publist_id: '6802'
quality_controlled: 0
status: public
title: Estimating the rate of irreversibility in protein evolution
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
volume: 4
year: '2012'
...
---
_id: '8463'
abstract:
- lang: eng
text: The 1H dipolar network, which is the major obstacle for applying proton detection
in the solid-state, can be reduced by deuteration, employing the RAP (Reduced
Adjoining Protonation) labeling scheme, which yields random protonation at non-exchangeable
sites. We present here a systematic study on the optimal degree of random sidechain
protonation in RAP samples as a function of the MAS (magic angle spinning) frequency.
In particular, we compare 1H sensitivity and linewidth of a microcrystalline protein,
the SH3 domain of chicken α-spectrin, for samples, prepared with 5–25 % H2O in
the E. coli growth medium, in the MAS frequency range of 20–60 kHz. At an external
field of 19.96 T (850 MHz), we find that using a proton concentration between
15 and 25 % in the M9 medium yields the best compromise in terms of sensitivity
and resolution, with an achievable average 1H linewidth on the order of 40–50
Hz. Comparing sensitivities at a MAS frequency of 60 versus 20 kHz, a gain in
sensitivity by a factor of 4–4.5 is observed in INEPT-based 1H detected 1D 1H,13C
correlation experiments. In total, we find that spectra recorded with a 1.3 mm
rotor at 60 kHz have almost the same sensitivity as spectra recorded with a fully
packed 3.2 mm rotor at 20 kHz, even though ~20× less material is employed. The
improved sensitivity is attributed to 1H line narrowing due to fast MAS and to
the increased efficiency of the 1.3 mm coil.
article_processing_charge: No
article_type: original
author:
- first_name: Sam
full_name: Asami, Sam
last_name: Asami
- first_name: Kathrin
full_name: Szekely, Kathrin
last_name: Szekely
- first_name: Paul
full_name: Schanda, Paul
id: 7B541462-FAF6-11E9-A490-E8DFE5697425
last_name: Schanda
orcid: 0000-0002-9350-7606
- first_name: Beat H.
full_name: Meier, Beat H.
last_name: Meier
- first_name: Bernd
full_name: Reif, Bernd
last_name: Reif
citation:
ama: Asami S, Szekely K, Schanda P, Meier BH, Reif B. Optimal degree of protonation
for 1H detection of aliphatic sites in randomly deuterated proteins as a function
of the MAS frequency. Journal of Biomolecular NMR. 2012;54(2):155-168.
doi:10.1007/s10858-012-9659-9
apa: Asami, S., Szekely, K., Schanda, P., Meier, B. H., & Reif, B. (2012). Optimal
degree of protonation for 1H detection of aliphatic sites in randomly deuterated
proteins as a function of the MAS frequency. Journal of Biomolecular NMR.
Springer Nature. https://doi.org/10.1007/s10858-012-9659-9
chicago: Asami, Sam, Kathrin Szekely, Paul Schanda, Beat H. Meier, and Bernd Reif.
“Optimal Degree of Protonation for 1H Detection of Aliphatic Sites in Randomly
Deuterated Proteins as a Function of the MAS Frequency.” Journal of Biomolecular
NMR. Springer Nature, 2012. https://doi.org/10.1007/s10858-012-9659-9.
ieee: S. Asami, K. Szekely, P. Schanda, B. H. Meier, and B. Reif, “Optimal degree
of protonation for 1H detection of aliphatic sites in randomly deuterated proteins
as a function of the MAS frequency,” Journal of Biomolecular NMR, vol.
54, no. 2. Springer Nature, pp. 155–168, 2012.
ista: Asami S, Szekely K, Schanda P, Meier BH, Reif B. 2012. Optimal degree of protonation
for 1H detection of aliphatic sites in randomly deuterated proteins as a function
of the MAS frequency. Journal of Biomolecular NMR. 54(2), 155–168.
mla: Asami, Sam, et al. “Optimal Degree of Protonation for 1H Detection of Aliphatic
Sites in Randomly Deuterated Proteins as a Function of the MAS Frequency.” Journal
of Biomolecular NMR, vol. 54, no. 2, Springer Nature, 2012, pp. 155–68, doi:10.1007/s10858-012-9659-9.
short: S. Asami, K. Szekely, P. Schanda, B.H. Meier, B. Reif, Journal of Biomolecular
NMR 54 (2012) 155–168.
date_created: 2020-09-18T10:09:18Z
date_published: 2012-08-23T00:00:00Z
date_updated: 2021-01-12T08:19:27Z
day: '23'
doi: 10.1007/s10858-012-9659-9
extern: '1'
intvolume: ' 54'
issue: '2'
language:
- iso: eng
month: '08'
oa_version: None
page: 155-168
publication: Journal of Biomolecular NMR
publication_identifier:
issn:
- 0925-2738
- 1573-5001
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
status: public
title: Optimal degree of protonation for 1H detection of aliphatic sites in randomly
deuterated proteins as a function of the MAS frequency
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 54
year: '2012'
...
---
_id: '8465'
abstract:
- lang: eng
text: We demonstrate that conformational exchange processes in proteins on microsecond-to-millisecond
time scales can be detected and quantified by solid-state NMR spectroscopy. We
show two independent approaches that measure the effect of conformational exchange
on transverse relaxation parameters, namely Carr–Purcell–Meiboom–Gill relaxation-dispersion
experiments and measurement of differential multiple-quantum coherence decay.
Long coherence lifetimes, as required for these experiments, are achieved by the
use of highly deuterated samples and fast magic-angle spinning. The usefulness
of the approaches is demonstrated by application to microcrystalline ubiquitin.
We detect a conformational exchange process in a region of the protein for which
dynamics have also been observed in solution. Interestingly, quantitative analysis
of the data reveals that the exchange process is more than 1 order of magnitude
slower than in solution, and this points to the impact of the crystalline environment
on free energy barriers.
article_processing_charge: No
article_type: original
author:
- first_name: Martin
full_name: Tollinger, Martin
last_name: Tollinger
- first_name: Astrid C.
full_name: Sivertsen, Astrid C.
last_name: Sivertsen
- first_name: Beat H.
full_name: Meier, Beat H.
last_name: Meier
- first_name: Matthias
full_name: Ernst, Matthias
last_name: Ernst
- first_name: Paul
full_name: Schanda, Paul
id: 7B541462-FAF6-11E9-A490-E8DFE5697425
last_name: Schanda
orcid: 0000-0002-9350-7606
citation:
ama: Tollinger M, Sivertsen AC, Meier BH, Ernst M, Schanda P. Site-resolved measurement
of microsecond-to-millisecond conformational-exchange processes in proteins by
solid-state NMR spectroscopy. Journal of the American Chemical Society.
2012;134(36):14800-14807. doi:10.1021/ja303591y
apa: Tollinger, M., Sivertsen, A. C., Meier, B. H., Ernst, M., & Schanda, P.
(2012). Site-resolved measurement of microsecond-to-millisecond conformational-exchange
processes in proteins by solid-state NMR spectroscopy. Journal of the American
Chemical Society. American Chemical Society. https://doi.org/10.1021/ja303591y
chicago: Tollinger, Martin, Astrid C. Sivertsen, Beat H. Meier, Matthias Ernst,
and Paul Schanda. “Site-Resolved Measurement of Microsecond-to-Millisecond Conformational-Exchange
Processes in Proteins by Solid-State NMR Spectroscopy.” Journal of the American
Chemical Society. American Chemical Society, 2012. https://doi.org/10.1021/ja303591y.
ieee: M. Tollinger, A. C. Sivertsen, B. H. Meier, M. Ernst, and P. Schanda, “Site-resolved
measurement of microsecond-to-millisecond conformational-exchange processes in
proteins by solid-state NMR spectroscopy,” Journal of the American Chemical
Society, vol. 134, no. 36. American Chemical Society, pp. 14800–14807, 2012.
ista: Tollinger M, Sivertsen AC, Meier BH, Ernst M, Schanda P. 2012. Site-resolved
measurement of microsecond-to-millisecond conformational-exchange processes in
proteins by solid-state NMR spectroscopy. Journal of the American Chemical Society.
134(36), 14800–14807.
mla: Tollinger, Martin, et al. “Site-Resolved Measurement of Microsecond-to-Millisecond
Conformational-Exchange Processes in Proteins by Solid-State NMR Spectroscopy.”
Journal of the American Chemical Society, vol. 134, no. 36, American Chemical
Society, 2012, pp. 14800–07, doi:10.1021/ja303591y.
short: M. Tollinger, A.C. Sivertsen, B.H. Meier, M. Ernst, P. Schanda, Journal of
the American Chemical Society 134 (2012) 14800–14807.
date_created: 2020-09-18T10:10:20Z
date_published: 2012-08-21T00:00:00Z
date_updated: 2021-01-12T08:19:27Z
day: '21'
doi: 10.1021/ja303591y
extern: '1'
intvolume: ' 134'
issue: '36'
language:
- iso: eng
month: '08'
oa_version: None
page: 14800-14807
publication: Journal of the American Chemical Society
publication_identifier:
issn:
- 0002-7863
- 1520-5126
publication_status: published
publisher: American Chemical Society
quality_controlled: '1'
status: public
title: Site-resolved measurement of microsecond-to-millisecond conformational-exchange
processes in proteins by solid-state NMR spectroscopy
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 134
year: '2012'
...