---
_id: '2624'
abstract:
- lang: eng
text: Metabotropic γ-aminobutyric acid receptors (GABABRs) are involved in modulation
of synaptic transmission and activity of cerebellar and thalamic neurons. We used
subtype-specific antibodies in pre- and postembedding immunohistochemistry combined
with three-dimensional reconstruction of labelled profiles and quantification
of immunoparticles to reveal the subcellular distribution of pre- and postsynaptic
GABABR1a/b and GABABR2 in the rat cerebellum and ventrobasal thalamus. GABABR1a/b
and R2 were extensively colocalized in most brain regions including the cerebellum
and thalamus. In the cerebellum, immunoreactivity for both subtypes was prevalent
in the molecular layer. The most intense immunoreactivity was found in Purkinje
cell spines with a high density of immunoparticles at extrasynaptic sites peaking
at around 240 nm from glutamatergic synapses between spines and parallel fibre
varicosities. This is in contrast to dendrites at sites around GABAergic synapses
where sparse and random distribution was found for both subtypes. In addition,
more than one-tenth of the synaptic membrane specialization of spine-parallel
fibre synapses were labelled at pre- or postsynaptic sites. Weak immunolabelling
for both subtypes was also seen in parallel fibres but only rarely in GABAergic
axons. In the ventrobasal thalamus, immunolabelling for both receptor subtypes
was intense over the dendritic field of thalamocortical cells. Electron microscopy
demonstrated an extrasynaptic localization of GABABR1a/b and R2 exclusively in
postsynaptic elements. Quantitative analysis further revealed the density of GABABR1a/b
around GABAergic synapses was higher than glutamatergic synapses on thalamocortical
cell dendrites. The distinct localization of GABABRs relative to synaptic sites
in the cerebellum and ventrobasal thalamus suggests that GABABRs differentially
regulate activity of different neuronal populations.
acknowledgement: This work was supported by research grants from the Ministry of Education,
Science, Sports and Culture of Japan, and the Japan Society for the Promotion of
Science (P96319). We thank Drs L. Zaborszky and R. Luján for their comments on the
manuscript, Dr M. Watanabe for kindly supplying us with GluRδ2 and AMPA GluR1 antibodies,
Dr R.E. Edwards for rabbit BNPI antibody, and J. Hatakeyama and S. Doi for technical
assistance.
article_processing_charge: No
article_type: original
author:
- first_name: Ákos
full_name: Kulik, Ákos
last_name: Kulik
- first_name: Kazuhiko
full_name: Nakadate, Kazuhiko
last_name: Nakadate
- first_name: Gábor
full_name: Nyíri, Gábor
last_name: Nyíri
- first_name: Takuya
full_name: Notomi, Takuya
last_name: Notomi
- first_name: Barbara
full_name: Malitschek, Barbara
last_name: Malitschek
- first_name: Bernhard
full_name: Bettler, Bernhard
last_name: Bettler
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
citation:
ama: Kulik Á, Nakadate K, Nyíri G, et al. Distinct localization of GABAB receptors
relative to synaptic sites in the rat cerebellum and ventrobasal thalamus. European
Journal of Neuroscience. 2002;15(2):291-307. doi:10.1046/j.0953-816x.2001.01855.x
apa: Kulik, Á., Nakadate, K., Nyíri, G., Notomi, T., Malitschek, B., Bettler, B.,
& Shigemoto, R. (2002). Distinct localization of GABAB receptors relative
to synaptic sites in the rat cerebellum and ventrobasal thalamus. European
Journal of Neuroscience. Wiley-Blackwell. https://doi.org/10.1046/j.0953-816x.2001.01855.x
chicago: Kulik, Ákos, Kazuhiko Nakadate, Gábor Nyíri, Takuya Notomi, Barbara Malitschek,
Bernhard Bettler, and Ryuichi Shigemoto. “Distinct Localization of GABAB Receptors
Relative to Synaptic Sites in the Rat Cerebellum and Ventrobasal Thalamus.” European
Journal of Neuroscience. Wiley-Blackwell, 2002. https://doi.org/10.1046/j.0953-816x.2001.01855.x.
ieee: Á. Kulik et al., “Distinct localization of GABAB receptors relative
to synaptic sites in the rat cerebellum and ventrobasal thalamus,” European
Journal of Neuroscience, vol. 15, no. 2. Wiley-Blackwell, pp. 291–307, 2002.
ista: Kulik Á, Nakadate K, Nyíri G, Notomi T, Malitschek B, Bettler B, Shigemoto
R. 2002. Distinct localization of GABAB receptors relative to synaptic sites in
the rat cerebellum and ventrobasal thalamus. European Journal of Neuroscience.
15(2), 291–307.
mla: Kulik, Ákos, et al. “Distinct Localization of GABAB Receptors Relative to Synaptic
Sites in the Rat Cerebellum and Ventrobasal Thalamus.” European Journal of
Neuroscience, vol. 15, no. 2, Wiley-Blackwell, 2002, pp. 291–307, doi:10.1046/j.0953-816x.2001.01855.x.
short: Á. Kulik, K. Nakadate, G. Nyíri, T. Notomi, B. Malitschek, B. Bettler, R.
Shigemoto, European Journal of Neuroscience 15 (2002) 291–307.
date_created: 2018-12-11T11:58:44Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-18T13:08:40Z
day: '01'
doi: 10.1046/j.0953-816x.2001.01855.x
extern: '1'
external_id:
pmid:
- '11849296'
intvolume: ' 15'
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 291 - 307
pmid: 1
publication: European Journal of Neuroscience
publication_identifier:
issn:
- 0953-816X
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4275'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Distinct localization of GABAB receptors relative to synaptic sites in the
rat cerebellum and ventrobasal thalamus
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 15
year: '2002'
...
---
_id: '2694'
abstract:
- lang: eng
text: We outline the status of rigorous derivations of certain classical evolution
equations as limits of Schrödinger dynamics. We explain two recent results jointly
with H.T. Yau in more details. The first one is the derivation of the linear Boltzmann
equation as the long time limit of the one-body Schrödinger equation with a random
potential. The second one is the mean field limit of high density bosons with
Coulomb interaction that leads to the nonlinear Hartree equation.
alternative_title:
- LNP
article_processing_charge: No
author:
- first_name: László
full_name: Erdös, László
id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
last_name: Erdös
orcid: 0000-0001-5366-9603
citation:
ama: 'Erdös L. Scaling limits of Schrödinger quantum mechanics. In: Dynamics
of Dissipation. Lecture Notes in Physics. Springer; 2002:487-506. doi:10.1007/3-540-46122-1_19'
apa: Erdös, L. (2002). Scaling limits of Schrödinger quantum mechanics. In Dynamics
of Dissipation (pp. 487–506). Springer. https://doi.org/10.1007/3-540-46122-1_19
chicago: Erdös, László. “Scaling Limits of Schrödinger Quantum Mechanics.” In Dynamics
of Dissipation, 487–506. Lecture Notes in Physics. Springer, 2002. https://doi.org/10.1007/3-540-46122-1_19.
ieee: L. Erdös, “Scaling limits of Schrödinger quantum mechanics,” in Dynamics
of Dissipation, Springer, 2002, pp. 487–506.
ista: 'Erdös L. 2002.Scaling limits of Schrödinger quantum mechanics. In: Dynamics
of Dissipation. LNP, , 487–506.'
mla: Erdös, László. “Scaling Limits of Schrödinger Quantum Mechanics.” Dynamics
of Dissipation, Springer, 2002, pp. 487–506, doi:10.1007/3-540-46122-1_19.
short: L. Erdös, in:, Dynamics of Dissipation, Springer, 2002, pp. 487–506.
conference:
name: '38th Winter School of Theoretical Physics : Dynamical Semigroups: Dissipation,
Chaos, Quanta'
date_created: 2018-12-11T11:59:06Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-18T10:23:18Z
day: '01'
doi: 10.1007/3-540-46122-1_19
extern: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 487 - 506
publication: Dynamics of Dissipation
publication_identifier:
isbn:
- '9783540441113'
publication_status: published
publisher: Springer
publist_id: '4203'
quality_controlled: '1'
series_title: Lecture Notes in Physics
status: public
title: Scaling limits of Schrödinger quantum mechanics
type: book_chapter
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
year: '2002'
...
---
_id: '2708'
alternative_title:
- Contemporary Mathematics
author:
- first_name: László
full_name: László Erdös
id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
last_name: Erdös
orcid: 0000-0001-5366-9603
citation:
ama: 'Erdös L. Two dimensional Pauli operator via scalar potential. In: Vol 307.
World Scientific Publishing; 2002:129-133. doi:10.1090/conm/307'
apa: 'Erdös, L. (2002). Two dimensional Pauli operator via scalar potential (Vol.
307, pp. 129–133). Presented at the QMath: Mathematical Results in Quantum Physics,
World Scientific Publishing. https://doi.org/10.1090/conm/307'
chicago: Erdös, László. “Two Dimensional Pauli Operator via Scalar Potential,” 307:129–33.
World Scientific Publishing, 2002. https://doi.org/10.1090/conm/307.
ieee: 'L. Erdös, “Two dimensional Pauli operator via scalar potential,” presented
at the QMath: Mathematical Results in Quantum Physics, 2002, vol. 307, pp. 129–133.'
ista: 'Erdös L. 2002. Two dimensional Pauli operator via scalar potential. QMath:
Mathematical Results in Quantum Physics, Contemporary Mathematics, vol. 307, 129–133.'
mla: Erdös, László. Two Dimensional Pauli Operator via Scalar Potential.
Vol. 307, World Scientific Publishing, 2002, pp. 129–33, doi:10.1090/conm/307.
short: L. Erdös, in:, World Scientific Publishing, 2002, pp. 129–133.
conference:
name: 'QMath: Mathematical Results in Quantum Physics'
date_created: 2018-12-11T11:59:11Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2021-01-12T06:59:11Z
day: '01'
doi: 10.1090/conm/307
extern: 1
intvolume: ' 307'
month: '01'
page: 129 - 133
publication_status: published
publisher: World Scientific Publishing
publist_id: '4188'
quality_controlled: 0
status: public
title: Two dimensional Pauli operator via scalar potential
type: conference
volume: 307
year: '2002'
...
---
_id: '2737'
abstract:
- lang: eng
text: We derive the time-dependent Schrödinger–Poisson equation as the weak coupling
limit of the N-body linear Schrödinger equation with Coulomb potential.
acknowledgement: "The authors thank the ESI in Vienna and the Austrian START project
“Nonlinear Schrödinger\r\nand quantum Boltzmann equations” of N.J.M. for hospitality
and support. Also, F.G. was supported by the Institut\r\nUniversitaire de France
and N.J.M. by the bilateral Austrian-French “AMADEUS” programme. H.-T.Y. and L.E.
were\r\nsupported by NSF Grants DMS-0072098 and DMS-9970323, respectively"
article_processing_charge: No
article_type: original
author:
- first_name: Claude
full_name: Bardos, Claude
last_name: Bardos
- first_name: László
full_name: Erdös, László
id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
last_name: Erdös
orcid: 0000-0001-5366-9603
- first_name: François
full_name: Golse, François
last_name: Golse
- first_name: Norbert
full_name: Mauser, Norbert
last_name: Mauser
- first_name: Horng
full_name: Yau, Horng
last_name: Yau
citation:
ama: Bardos C, Erdös L, Golse F, Mauser N, Yau H. Derivation of the Schrödinger-Poisson
equation from the quantum N-body problem. Comptes Rendus Mathematique.
2002;334(6):515-520. doi:10.1016/S1631-073X(02)02253-7
apa: Bardos, C., Erdös, L., Golse, F., Mauser, N., & Yau, H. (2002). Derivation
of the Schrödinger-Poisson equation from the quantum N-body problem. Comptes
Rendus Mathematique. Elsevier. https://doi.org/10.1016/S1631-073X(02)02253-7
chicago: Bardos, Claude, László Erdös, François Golse, Norbert Mauser, and Horng
Yau. “Derivation of the Schrödinger-Poisson Equation from the Quantum N-Body Problem.”
Comptes Rendus Mathematique. Elsevier, 2002. https://doi.org/10.1016/S1631-073X(02)02253-7.
ieee: C. Bardos, L. Erdös, F. Golse, N. Mauser, and H. Yau, “Derivation of the Schrödinger-Poisson
equation from the quantum N-body problem,” Comptes Rendus Mathematique,
vol. 334, no. 6. Elsevier, pp. 515–520, 2002.
ista: Bardos C, Erdös L, Golse F, Mauser N, Yau H. 2002. Derivation of the Schrödinger-Poisson
equation from the quantum N-body problem. Comptes Rendus Mathematique. 334(6),
515–520.
mla: Bardos, Claude, et al. “Derivation of the Schrödinger-Poisson Equation from
the Quantum N-Body Problem.” Comptes Rendus Mathematique, vol. 334, no.
6, Elsevier, 2002, pp. 515–20, doi:10.1016/S1631-073X(02)02253-7.
short: C. Bardos, L. Erdös, F. Golse, N. Mauser, H. Yau, Comptes Rendus Mathematique
334 (2002) 515–520.
date_created: 2018-12-11T11:59:20Z
date_published: 2002-03-30T00:00:00Z
date_updated: 2023-07-18T09:24:24Z
day: '30'
doi: 10.1016/S1631-073X(02)02253-7
extern: '1'
intvolume: ' 334'
issue: '6'
language:
- iso: eng
month: '03'
oa_version: None
page: 515 - 520
publication: Comptes Rendus Mathematique
publication_identifier:
issn:
- 1631-073X
publication_status: published
publisher: Elsevier
publist_id: '4155'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Derivation of the Schrödinger-Poisson equation from the quantum N-body problem
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 334
year: '2002'
...
---
_id: '2738'
abstract:
- lang: eng
text: We consider the long time evolution of a quantum particle weakly interacting
with a phonon field. We show that in the weak coupling limit the Wigner distribution
of the electron density matrix converges to the solution of the linear Boltzmann
equation globally in time. The collision kernel is identified as the sum of an
emission and an absorption term that depend on the equilibrium distribution of
the free phonon modes.
acknowledgement: "This work initially was a joint project with H.-T. Yau and several
ideas\r\npresented here have been developed in collaboration with him. I would like\r\nto
thank him for the invaluable discussions and encouragement through\r\nthe entire
work. Part of this project was completed during several visits at\r\nthe Erwin Schrödinger
Institute, Vienna, and at the Center of Theoretical\r\nStudies, Hsinchu, Taiwan.
The author is grateful for the hospitality and\r\nfinancial support. This work was
partially supported by NSF Grant DMS9970323."
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: László
full_name: Erdös, László
id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
last_name: Erdös
orcid: 0000-0001-5366-9603
citation:
ama: Erdös L. Linear Boltzmann equation as the long time dynamics of an electron
weakly coupled to a phonon field. Journal of Statistical Physics. 2002;107(5-6):1043-1127.
doi:10.1023/A:1015157624384
apa: Erdös, L. (2002). Linear Boltzmann equation as the long time dynamics of an
electron weakly coupled to a phonon field. Journal of Statistical Physics.
Springer. https://doi.org/10.1023/A:1015157624384
chicago: Erdös, László. “Linear Boltzmann Equation as the Long Time Dynamics of
an Electron Weakly Coupled to a Phonon Field.” Journal of Statistical Physics.
Springer, 2002. https://doi.org/10.1023/A:1015157624384.
ieee: L. Erdös, “Linear Boltzmann equation as the long time dynamics of an electron
weakly coupled to a phonon field,” Journal of Statistical Physics, vol.
107, no. 5–6. Springer, pp. 1043–1127, 2002.
ista: Erdös L. 2002. Linear Boltzmann equation as the long time dynamics of an electron
weakly coupled to a phonon field. Journal of Statistical Physics. 107(5–6), 1043–1127.
mla: Erdös, László. “Linear Boltzmann Equation as the Long Time Dynamics of an Electron
Weakly Coupled to a Phonon Field.” Journal of Statistical Physics, vol.
107, no. 5–6, Springer, 2002, pp. 1043–127, doi:10.1023/A:1015157624384.
short: L. Erdös, Journal of Statistical Physics 107 (2002) 1043–1127.
date_created: 2018-12-11T11:59:20Z
date_published: 2002-06-01T00:00:00Z
date_updated: 2023-07-18T09:08:45Z
day: '01'
doi: 10.1023/A:1015157624384
extern: '1'
external_id:
arxiv:
- math-ph/0108025
intvolume: ' 107'
issue: 5-6
language:
- iso: eng
month: '06'
oa_version: Submitted Version
page: 1043 - 1127
publication: Journal of Statistical Physics
publication_identifier:
issn:
- 0022-4715
publication_status: published
publisher: Springer
publist_id: '4154'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Linear Boltzmann equation as the long time dynamics of an electron weakly coupled
to a phonon field
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 107
year: '2002'
...
---
_id: '2739'
abstract:
- lang: eng
text: We define the two dimensional Pauli operator and identify its core for magnetic
fields that are regular Borel measures. The magnetic field is generated by a scalar
potential hence we bypass the usual A L 2loc condition on the vector potential,
which does not allow to consider such singular fields. We extend the Aharonov-Casher
theorem for magnetic fields that are measures with finite total variation and
we present a counterexample in case of infinite total variation. One of the key
technical tools is a weighted L 2 estimate on a singular integral operator.
acknowledgement: "This work started during the first author’s visit at the Erwin Schrödinger
Institute, Vienna.\r\nValuable discussions with T. Hoffmann-Ostenhof and M. Loss
are gratefully acknowledged. The authors thank\r\nthe referee for careful reading
and comments"
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: László
full_name: Erdös, László
id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
last_name: Erdös
orcid: 0000-0001-5366-9603
- first_name: Vitali
full_name: Vougalter, Vitali
last_name: Vougalter
citation:
ama: Erdös L, Vougalter V. Pauli operator and Aharonov–Casher theorem¶ for measure
valued magnetic fields. Communications in Mathematical Physics. 2002;225(2):399-421.
doi:10.1007/s002200100585
apa: Erdös, L., & Vougalter, V. (2002). Pauli operator and Aharonov–Casher theorem¶
for measure valued magnetic fields. Communications in Mathematical Physics.
Springer. https://doi.org/10.1007/s002200100585
chicago: Erdös, László, and Vitali Vougalter. “Pauli Operator and Aharonov–Casher
Theorem¶ for Measure Valued Magnetic Fields.” Communications in Mathematical
Physics. Springer, 2002. https://doi.org/10.1007/s002200100585.
ieee: L. Erdös and V. Vougalter, “Pauli operator and Aharonov–Casher theorem¶ for
measure valued magnetic fields,” Communications in Mathematical Physics,
vol. 225, no. 2. Springer, pp. 399–421, 2002.
ista: Erdös L, Vougalter V. 2002. Pauli operator and Aharonov–Casher theorem¶ for
measure valued magnetic fields. Communications in Mathematical Physics. 225(2),
399–421.
mla: Erdös, László, and Vitali Vougalter. “Pauli Operator and Aharonov–Casher Theorem¶
for Measure Valued Magnetic Fields.” Communications in Mathematical Physics,
vol. 225, no. 2, Springer, 2002, pp. 399–421, doi:10.1007/s002200100585.
short: L. Erdös, V. Vougalter, Communications in Mathematical Physics 225 (2002)
399–421.
date_created: 2018-12-11T11:59:21Z
date_published: 2002-02-01T00:00:00Z
date_updated: 2023-07-18T08:57:54Z
day: '01'
doi: 10.1007/s002200100585
extern: '1'
external_id:
arxiv:
- math-ph/0109015v1
intvolume: ' 225'
issue: '2'
language:
- iso: eng
month: '02'
oa_version: None
page: 399 - 421
publication: Communications in Mathematical Physics
publication_identifier:
issn:
- 0010-3616
publication_status: published
publisher: Springer
publist_id: '4153'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Pauli operator and Aharonov–Casher theorem¶ for measure valued magnetic fields
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 225
year: '2002'
...
---
_id: '2740'
abstract:
- lang: eng
text: We show that the lowest eigenvalue of the magnetic Schrödinger operator on
a line bundle over a compact Riemann surface M is bounded by the L1-norm of the
magnetic field B. This implies a similar bound on the multiplicity of the ground
state. An example shows that this degeneracy can indeed be comparable with ∫M
|B| even in case of the trivial bundle.
article_processing_charge: No
article_type: original
author:
- first_name: László
full_name: Erdös, László
id: 4DBD5372-F248-11E8-B48F-1D18A9856A87
last_name: Erdös
orcid: 0000-0001-5366-9603
citation:
ama: Erdös L. Spectral shift and multiplicity of the first eigenvalue of the magnetic
Schrödinger operator in two dimensions. Annales de l’Institut Fourier.
2002;52(6):1833-1874. doi:10.5802/aif.1936
apa: Erdös, L. (2002). Spectral shift and multiplicity of the first eigenvalue of
the magnetic Schrödinger operator in two dimensions. Annales de l’Institut
Fourier. Association des Annales de l’Institut Fourier. https://doi.org/10.5802/aif.1936
chicago: Erdös, László. “Spectral Shift and Multiplicity of the First Eigenvalue
of the Magnetic Schrödinger Operator in Two Dimensions.” Annales de l’Institut
Fourier. Association des Annales de l’Institut Fourier, 2002. https://doi.org/10.5802/aif.1936.
ieee: L. Erdös, “Spectral shift and multiplicity of the first eigenvalue of the
magnetic Schrödinger operator in two dimensions,” Annales de l’Institut Fourier,
vol. 52, no. 6. Association des Annales de l’Institut Fourier, pp. 1833–1874,
2002.
ista: Erdös L. 2002. Spectral shift and multiplicity of the first eigenvalue of
the magnetic Schrödinger operator in two dimensions. Annales de l’Institut Fourier.
52(6), 1833–1874.
mla: Erdös, László. “Spectral Shift and Multiplicity of the First Eigenvalue of
the Magnetic Schrödinger Operator in Two Dimensions.” Annales de l’Institut
Fourier, vol. 52, no. 6, Association des Annales de l’Institut Fourier, 2002,
pp. 1833–74, doi:10.5802/aif.1936.
short: L. Erdös, Annales de l’Institut Fourier 52 (2002) 1833–1874.
date_created: 2018-12-11T11:59:21Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-18T08:38:34Z
day: '01'
doi: 10.5802/aif.1936
extern: '1'
intvolume: ' 52'
issue: '6'
language:
- iso: eng
month: '01'
oa_version: None
page: 1833-1874
publication: Annales de l'Institut Fourier
publication_identifier:
issn:
- 0373-0956
publication_status: published
publisher: Association des Annales de l'Institut Fourier
publist_id: '4152'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Spectral shift and multiplicity of the first eigenvalue of the magnetic Schrödinger
operator in two dimensions
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 52
year: '2002'
...
---
_id: '2866'
abstract:
- lang: eng
text: 'Developmental responses to the plant hormone auxin are thought to be mediated
by interacting pairs from two protein families: short-lived inhibitory IAA proteins
and ARF transcription factors binding to auxin-response elements. Monopteros mutants
lacking activating ARF5 and the auxin-insensitive mutant bodenlos fail to initiate
the root meristem during early embryogenesis. Here we show that the bodenlos phenotype
results from an amino-acid exchange in the conserved degradation domain of IAA12.
BODENLOS and MONOPTEROS interact in the yeast two-hybrid assay and the two genes
are coexpressed in early embryogenesis, suggesting that BODENLOS inhibits MONOPTEROS
action in root meristem initiation.'
acknowledgement: "We thank C. Maulbetsch for isolating BDL cDNA clones; T. Berleth
and J. Friml for providing clones for in situ probes; K. Harter for making available
the parsley protoplast system; and J. Friml, N. Geldner, M. Griffith, C. Schwechheimer,
D. Weigel, and D. Weijers for helpful comments and critical reading of the manuscript.
This work was supported by Sonderforschungsbereich 446 “Mechanismen des Zellverhaltens
bei Eukaryoten.”\r\n\r\nThe publication costs of this article were defrayed in part
by payment of page charges. This article must therefore be hereby marked “advertisement”
in accordance with 18 USC section 1734 solely to indicate this fact."
article_processing_charge: No
article_type: original
author:
- first_name: Thorsten
full_name: Hamann, Thorsten
last_name: Hamann
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Isabel
full_name: Bäurle, Isabel
last_name: Bäurle
- first_name: Marika
full_name: Kientz, Marika
last_name: Kientz
- first_name: Gerd
full_name: Jürgens, Gerd
last_name: Jürgens
citation:
ama: Hamann T, Benková E, Bäurle I, Kientz M, Jürgens G. The Arabidopsis BODENLOS
gene encodes an auxin response protein inhibiting MONOPTEROS-mediated embryo patterning.
Genes and Development. 2002;16(13):1610-1615. doi:10.1101/gad.229402
apa: Hamann, T., Benková, E., Bäurle, I., Kientz, M., & Jürgens, G. (2002).
The Arabidopsis BODENLOS gene encodes an auxin response protein inhibiting MONOPTEROS-mediated
embryo patterning. Genes and Development. Cold Spring Harbor Laboratory
Press. https://doi.org/10.1101/gad.229402
chicago: Hamann, Thorsten, Eva Benková, Isabel Bäurle, Marika Kientz, and Gerd Jürgens.
“The Arabidopsis BODENLOS Gene Encodes an Auxin Response Protein Inhibiting MONOPTEROS-Mediated
Embryo Patterning.” Genes and Development. Cold Spring Harbor Laboratory
Press, 2002. https://doi.org/10.1101/gad.229402.
ieee: T. Hamann, E. Benková, I. Bäurle, M. Kientz, and G. Jürgens, “The Arabidopsis
BODENLOS gene encodes an auxin response protein inhibiting MONOPTEROS-mediated
embryo patterning,” Genes and Development, vol. 16, no. 13. Cold Spring
Harbor Laboratory Press, pp. 1610–1615, 2002.
ista: Hamann T, Benková E, Bäurle I, Kientz M, Jürgens G. 2002. The Arabidopsis
BODENLOS gene encodes an auxin response protein inhibiting MONOPTEROS-mediated
embryo patterning. Genes and Development. 16(13), 1610–1615.
mla: Hamann, Thorsten, et al. “The Arabidopsis BODENLOS Gene Encodes an Auxin Response
Protein Inhibiting MONOPTEROS-Mediated Embryo Patterning.” Genes and Development,
vol. 16, no. 13, Cold Spring Harbor Laboratory Press, 2002, pp. 1610–15, doi:10.1101/gad.229402.
short: T. Hamann, E. Benková, I. Bäurle, M. Kientz, G. Jürgens, Genes and Development
16 (2002) 1610–1615.
date_created: 2018-12-11T12:00:01Z
date_published: 2002-07-01T00:00:00Z
date_updated: 2023-07-18T08:26:58Z
day: '01'
doi: 10.1101/gad.229402
extern: '1'
external_id:
pmid:
- '12101120'
intvolume: ' 16'
issue: '13'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC186366/
month: '07'
oa: 1
oa_version: Published Version
page: 1610 - 1615
pmid: 1
publication: Genes and Development
publication_identifier:
issn:
- 0890-9369
publication_status: published
publisher: Cold Spring Harbor Laboratory Press
publist_id: '3921'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Arabidopsis BODENLOS gene encodes an auxin response protein inhibiting
MONOPTEROS-mediated embryo patterning
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 16
year: '2002'
...
---
_id: '2927'
abstract:
- lang: eng
text: 'In the last few years, several new algorithms based on graph cuts have been
developed to solve energy minimization problems in computer vision. Each of these
techniques constructs a graph such that the minimum cut on the graph also minimizes
the energy. Yet because these graph constructions are complex and highly specific
to a particular energy function, graph cuts have seen limited application to date.
In this paper we characterize the energy functions that can be minimized by graph
cuts. Our results are restricted to energy functions with binary variables. However,
our work generalizes many previous constructions, and is easily applicable to
vision problems that involve large numbers of labels, such as stereo, motion,
image restoration and scene reconstruction. We present three main results: a necessary
condition for any energy function that can be minimized by graph cuts; a sufficient
condition for energy functions that can be written as a sum of functions of up
to three variables at a time; and a general-purpose construction to minimize such
an energy function. Researchers who are considering the use of graph cuts to optimize
a particular energy function can use our results to determine if this is possible,
and then follow our construction to create the appropriate graph.'
acknowledgement: We thank Olga Veksler and Yuri Boykov for their careful reading of
this paper, and for valuable comments which greatly improved itsreadibility. We
also thank Ian Jermyn for helping us clarify the paper’s motivation. This research
was supported by NSF grants IIS-9900115 and CCR-0113371, and by a grant from Microsoft
Research.
article_processing_charge: No
author:
- first_name: Vladimir
full_name: Kolmogorov, Vladimir
id: 3D50B0BA-F248-11E8-B48F-1D18A9856A87
last_name: Kolmogorov
- first_name: Ramin
full_name: Zabih, Ramin
last_name: Zabih
citation:
ama: 'Kolmogorov V, Zabih R. Multi-camera scene reconstruction via graph cuts. In:
Proceedings of the 7th European Conference on Computer Vision. Springer;
2002:65-81. doi:10.1007/3-540-47977-5_5'
apa: 'Kolmogorov, V., & Zabih, R. (2002). Multi-camera scene reconstruction
via graph cuts. In Proceedings of the 7th European Conference on Computer Vision
(pp. 65–81). Copenhagen, Denmark: Springer. https://doi.org/10.1007/3-540-47977-5_5'
chicago: Kolmogorov, Vladimir, and Ramin Zabih. “Multi-Camera Scene Reconstruction
via Graph Cuts.” In Proceedings of the 7th European Conference on Computer
Vision, 65–81. Springer, 2002. https://doi.org/10.1007/3-540-47977-5_5.
ieee: V. Kolmogorov and R. Zabih, “Multi-camera scene reconstruction via graph cuts,”
in Proceedings of the 7th European Conference on Computer Vision, Copenhagen,
Denmark, 2002, pp. 65–81.
ista: 'Kolmogorov V, Zabih R. 2002. Multi-camera scene reconstruction via graph
cuts. Proceedings of the 7th European Conference on Computer Vision. ECCV: European
Conference on Computer Vision, 65–81.'
mla: Kolmogorov, Vladimir, and Ramin Zabih. “Multi-Camera Scene Reconstruction via
Graph Cuts.” Proceedings of the 7th European Conference on Computer Vision,
Springer, 2002, pp. 65–81, doi:10.1007/3-540-47977-5_5.
short: V. Kolmogorov, R. Zabih, in:, Proceedings of the 7th European Conference
on Computer Vision, Springer, 2002, pp. 65–81.
conference:
end_date: 2002-05-31
location: Copenhagen, Denmark
name: 'ECCV: European Conference on Computer Vision'
start_date: 2002-05-28
date_created: 2018-12-11T12:00:23Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-18T08:20:02Z
day: '01'
doi: 10.1007/3-540-47977-5_5
extern: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 65 - 81
publication: Proceedings of the 7th European Conference on Computer Vision
publication_identifier:
isbn:
- '9783540437468'
publication_status: published
publisher: Springer
publist_id: '3810'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multi-camera scene reconstruction via graph cuts
type: conference
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
year: '2002'
...
---
_id: '2986'
abstract:
- lang: eng
text: Long-standing models propose that plant growth responses to light or gravity
are mediated by asymmetric distribution of the phytohormone auxin. Physiological
studies implicated a specific transport system that relocates auxin laterally,
thereby effecting differential growth; however, neither the molecular components
of this system nor the cellular mechanism of auxin redistribution on light or
gravity perception have been identified. Here, we show that auxin accumulates
asymmetrically during differential growth in an efflux-dependent manner. Mutations
in the Arabidopsis gene PIN3, a regulator of auxin efflux, alter differential
growth. PIN3 is expressed in gravity-sensing tissues, with PIN3 protein accumulating
predominantly at the lateral cell surface. PIN3 localizes to the plasma membrane
and to vesicles that cycle in an actin-dependent manner. In the root columella,
PIN3 is positioned symmetrically at the plasma membrane but rapidly relocalizes
laterally on gravity stimulation. Our data indicate that PIN3 is a component of
the lateral auxin transport system regulating tropic growth. In addition, actin-dependent
relocalization of PIN3 in response to gravity provides a mechanism for redirecting
auxin flux to trigger asymmetric growth.
acknowledgement: We thank G. Jürgens for enabling J.F. to accomplish part of this
work in his laboratory; P. Tänzler and M. Sauer for technical assistance; H. Vahlenkamp
for technical assistance in immunocytochemistry; M. Estelle for providing material
and suggestions; T. Altman for BAC filter sets; the ADIS (Automated DNA Isolation
and Sequencing) service group for DNA sequencing; ZIGIA (Center for Functional Genomics
in Arabidopsis) for the En lines; and N. Geldner, T. Hamann, G. Jürgens, K. Schrick
and C. Schwechheimer for comments and critical reading of the manuscript. This work
was supported by a fellowship of the DAAD (J.F.), the DFG (Schwerpunktprogramm Phytohormone),
the Fonds der chemischen Industrie, the European Communities Biotechnology Programs,
the INCO-Copernicus Program and the European Space Agency MAP-Biotechnology Programme
article_processing_charge: No
article_type: original
author:
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Justyna
full_name: Wiśniewska, Justyna
last_name: Wiśniewska
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Kurt
full_name: Mendgen, Kurt
last_name: Mendgen
- first_name: Klaus
full_name: Palme, Klaus
last_name: Palme
citation:
ama: Friml J, Wiśniewska J, Benková E, Mendgen K, Palme K. Lateral relocation of
auxin efflux regulator PIN3 mediates tropism in Arabidopsis. Nature. 2002;415(6873):806-809.
doi:10.1038/415806a
apa: Friml, J., Wiśniewska, J., Benková, E., Mendgen, K., & Palme, K. (2002).
Lateral relocation of auxin efflux regulator PIN3 mediates tropism in Arabidopsis.
Nature. Nature Publishing Group. https://doi.org/10.1038/415806a
chicago: Friml, Jiří, Justyna Wiśniewska, Eva Benková, Kurt Mendgen, and Klaus Palme.
“Lateral Relocation of Auxin Efflux Regulator PIN3 Mediates Tropism in Arabidopsis.”
Nature. Nature Publishing Group, 2002. https://doi.org/10.1038/415806a.
ieee: J. Friml, J. Wiśniewska, E. Benková, K. Mendgen, and K. Palme, “Lateral relocation
of auxin efflux regulator PIN3 mediates tropism in Arabidopsis,” Nature,
vol. 415, no. 6873. Nature Publishing Group, pp. 806–809, 2002.
ista: Friml J, Wiśniewska J, Benková E, Mendgen K, Palme K. 2002. Lateral relocation
of auxin efflux regulator PIN3 mediates tropism in Arabidopsis. Nature. 415(6873),
806–809.
mla: Friml, Jiří, et al. “Lateral Relocation of Auxin Efflux Regulator PIN3 Mediates
Tropism in Arabidopsis.” Nature, vol. 415, no. 6873, Nature Publishing
Group, 2002, pp. 806–09, doi:10.1038/415806a.
short: J. Friml, J. Wiśniewska, E. Benková, K. Mendgen, K. Palme, Nature 415 (2002)
806–809.
date_created: 2018-12-11T12:00:42Z
date_published: 2002-02-14T00:00:00Z
date_updated: 2023-07-18T07:30:27Z
day: '14'
doi: 10.1038/415806a
extern: '1'
external_id:
pmid:
- '11845211 '
intvolume: ' 415'
issue: '6873'
language:
- iso: eng
month: '02'
oa_version: None
page: 806 - 809
pmid: 1
publication: Nature
publication_identifier:
issn:
- 0028-0836
publication_status: published
publisher: Nature Publishing Group
publist_id: '3715'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Lateral relocation of auxin efflux regulator PIN3 mediates tropism in Arabidopsis
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 415
year: '2002'
...
---
_id: '2987'
abstract:
- lang: eng
text: The hydra mutants of Arabidopsis are characterized by a pleiotropic phenotype
that shows defective embryonic and seedling cell patterning, morphogenesis, and
root growth. We demonstrate that the HYDRA1 gene encodes a Δ8-Δ7 sterol isomerase,
whereas HYDRA2 encodes a sterol C14 reductase, previously identified as the FACKEL
gene product. Seedlings mutant for each gene are similarly defective in the concentrations
of the three major Arabidopsis sterols. Promoter::reporter gene analysis showed
misexpression of the auxin-regulated DR5 and ACS1 promoters and of the epidermal
cell file-specific GL2 promoter in the mutants. The mutants exhibit enhanced responses
to auxin. The phenotypes can be rescued partially by inhibition of auxin and ethylene
signaling but not by exogenous sterols or brassinosteroids. We propose a model
in which correct sterol profiles are required for regulated auxin and ethylene
signaling through effects on membrane function.
acknowledgement: We thank Dr. Ken Feldmann for providing prospective hyd alleles,
Dr. Jane Murfett for providing DR5::GUS seed, Dr. D. Van Der Straeten for providing
ACS1::GUS seed, Dr. John Schiefelbein for providing GL2::GFP seed, and Dr. Ottoline
Leyser for axr1-12 and axr3-1 seed. etr1 and fk seed was obtained from the Nottingham
Arabidopsis Stock Centre. This work was supported by a Biotechnology and Biological
Science Research Council research studentship to M.S., a Durham University studentship
to M.P., and Biotechnology and Biological Science Research Council Grant 12/P02330
to J.T.
article_processing_charge: No
article_type: original
author:
- first_name: Martin
full_name: Souter, Martin
last_name: Souter
- first_name: Jennifer
full_name: Topping, Jennifer
last_name: Topping
- first_name: Margaret
full_name: Pullen, Margaret
last_name: Pullen
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Klaus
full_name: Palme, Klaus
last_name: Palme
- first_name: Rachel
full_name: Hackett, Rachel
last_name: Hackett
- first_name: Don
full_name: Grierson, Don
last_name: Grierson
- first_name: Keith
full_name: Lindsey, Keith
last_name: Lindsey
citation:
ama: Souter M, Topping J, Pullen M, et al. Hydra mutants of Arabidopsis are defective
in sterol profiles and auxin and ethylene signaling. Plant Cell. 2002;14(5):1017-1031.
doi:10.1105/tpc.001248
apa: Souter, M., Topping, J., Pullen, M., Friml, J., Palme, K., Hackett, R., … Lindsey,
K. (2002). Hydra mutants of Arabidopsis are defective in sterol profiles and auxin
and ethylene signaling. Plant Cell. American Society of Plant Biologists.
https://doi.org/10.1105/tpc.001248
chicago: Souter, Martin, Jennifer Topping, Margaret Pullen, Jiří Friml, Klaus Palme,
Rachel Hackett, Don Grierson, and Keith Lindsey. “Hydra Mutants of Arabidopsis
Are Defective in Sterol Profiles and Auxin and Ethylene Signaling.” Plant Cell.
American Society of Plant Biologists, 2002. https://doi.org/10.1105/tpc.001248.
ieee: M. Souter et al., “Hydra mutants of Arabidopsis are defective in sterol
profiles and auxin and ethylene signaling,” Plant Cell, vol. 14, no. 5.
American Society of Plant Biologists, pp. 1017–1031, 2002.
ista: Souter M, Topping J, Pullen M, Friml J, Palme K, Hackett R, Grierson D, Lindsey
K. 2002. Hydra mutants of Arabidopsis are defective in sterol profiles and auxin
and ethylene signaling. Plant Cell. 14(5), 1017–1031.
mla: Souter, Martin, et al. “Hydra Mutants of Arabidopsis Are Defective in Sterol
Profiles and Auxin and Ethylene Signaling.” Plant Cell, vol. 14, no. 5,
American Society of Plant Biologists, 2002, pp. 1017–31, doi:10.1105/tpc.001248.
short: M. Souter, J. Topping, M. Pullen, J. Friml, K. Palme, R. Hackett, D. Grierson,
K. Lindsey, Plant Cell 14 (2002) 1017–1031.
date_created: 2018-12-11T12:00:42Z
date_published: 2002-05-01T00:00:00Z
date_updated: 2023-07-18T07:34:32Z
day: '01'
doi: 10.1105/tpc.001248
extern: '1'
external_id:
pmid:
- '12034894'
intvolume: ' 14'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC150604/
month: '05'
oa: 1
oa_version: None
page: 1017 - 1031
pmid: 1
publication: Plant Cell
publication_identifier:
issn:
- 1040-4651
publication_status: published
publisher: American Society of Plant Biologists
publist_id: '3716'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Hydra mutants of Arabidopsis are defective in sterol profiles and auxin and
ethylene signaling
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 14
year: '2002'
...
---
_id: '2988'
abstract:
- lang: eng
text: Coordination of cell and tissue polarity commonly involves directional signaling
[1]. In the Arabidopsis root epidermis, cell polarity is revealed by basal, root
tip-oriented, hair outgrowth from hair-forming cells (trichoblasts) [2]. The plant
hormone auxin displays polar movements [1, 3] and accumulates at maximum concentration
in the root tip [4, 5]. The application of polar auxin transport inhibitors [3]
evokes changes in trichoblast polarity only at high concentrations and after long-term
application [2, 4]. Thus, it remains open whether components of the auxin transport
machinery mediate establishment of trichoblast polarity. Here we report that the
presumptive auxin influx carrier AUX1 [6, 7] contributes to apical-basal hair
cell polarity. AUX1 function is required for polarity changes induced by exogenous
application of the auxin 2,4-D, a preferential influx carrier substrate. Similar
to aux1 mutants, the vesicle trafficking inhibitor brefeldin A (BFA) interferes
with polar hair initiation, and AUX1 function is required for BFA-mediated polarity
changes. Consistently, BFA inhibits membrane trafficking of AUX1, trichoblast
hyperpolarization induced by 2,4-D, and alters the distal auxin maximum. Our results
identify AUX1 as one component of a novel BFA-sensitive auxin transport pathway
polarizing cells toward a hormone maximum.
article_processing_charge: No
article_type: original
author:
- first_name: Markus
full_name: Grebe, Markus
last_name: Grebe
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Ranjan
full_name: Swarup, Ranjan
last_name: Swarup
- first_name: Karin
full_name: Ljung, Karin
last_name: Ljung
- first_name: Göran
full_name: Sandberg, Göran
last_name: Sandberg
- first_name: Maarten
full_name: Terlou, Maarten
last_name: Terlou
- first_name: Klaus
full_name: Palme, Klaus
last_name: Palme
- first_name: Malcolm
full_name: Bennett, Malcolm
last_name: Bennett
- first_name: Ben
full_name: Scheres, Ben
last_name: Scheres
citation:
ama: Grebe M, Friml J, Swarup R, et al. Cell polarity signaling in Arabidopsis involves
a BFA sensitive auxin influx pathway. Current Biology. 2002;12(4):329-334.
doi:10.1016/S0960-9822(02)00654-1
apa: Grebe, M., Friml, J., Swarup, R., Ljung, K., Sandberg, G., Terlou, M., … Scheres,
B. (2002). Cell polarity signaling in Arabidopsis involves a BFA sensitive auxin
influx pathway. Current Biology. Cell Press. https://doi.org/10.1016/S0960-9822(02)00654-1
chicago: Grebe, Markus, Jiří Friml, Ranjan Swarup, Karin Ljung, Göran Sandberg,
Maarten Terlou, Klaus Palme, Malcolm Bennett, and Ben Scheres. “Cell Polarity
Signaling in Arabidopsis Involves a BFA Sensitive Auxin Influx Pathway.” Current
Biology. Cell Press, 2002. https://doi.org/10.1016/S0960-9822(02)00654-1.
ieee: M. Grebe et al., “Cell polarity signaling in Arabidopsis involves a
BFA sensitive auxin influx pathway,” Current Biology, vol. 12, no. 4. Cell
Press, pp. 329–334, 2002.
ista: Grebe M, Friml J, Swarup R, Ljung K, Sandberg G, Terlou M, Palme K, Bennett
M, Scheres B. 2002. Cell polarity signaling in Arabidopsis involves a BFA sensitive
auxin influx pathway. Current Biology. 12(4), 329–334.
mla: Grebe, Markus, et al. “Cell Polarity Signaling in Arabidopsis Involves a BFA
Sensitive Auxin Influx Pathway.” Current Biology, vol. 12, no. 4, Cell
Press, 2002, pp. 329–34, doi:10.1016/S0960-9822(02)00654-1.
short: M. Grebe, J. Friml, R. Swarup, K. Ljung, G. Sandberg, M. Terlou, K. Palme,
M. Bennett, B. Scheres, Current Biology 12 (2002) 329–334.
date_created: 2018-12-11T12:00:43Z
date_published: 2002-02-19T00:00:00Z
date_updated: 2023-07-17T12:15:28Z
day: '19'
doi: 10.1016/S0960-9822(02)00654-1
extern: '1'
external_id:
pmid:
- '11864575'
intvolume: ' 12'
issue: '4'
language:
- iso: eng
month: '02'
oa_version: None
page: 329 - 334
pmid: 1
publication: Current Biology
publication_identifier:
issn:
- 0960-9822
publication_status: published
publisher: Cell Press
publist_id: '3714'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Cell polarity signaling in Arabidopsis involves a BFA sensitive auxin influx
pathway
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 12
year: '2002'
...
---
_id: '2989'
abstract:
- lang: eng
text: In contrast to animals, little is known about pattern formation in plants.
Physiological and genetic data suggest the involvement of the phytohormone auxin
in this process. Here, we characterize a novel member of the PIN family of putative
auxin efflux carriers, Arabidopsis PIN4, that is localized in developing and mature
root meristems. Atpin4 mutants are defective in establishment and maintenance
of endogenous auxin gradients, fail to canalize externally applied auxin, and
display various patterning defects in both embryonic and seedling roots. We propose
a role for AtPIN4 in generating a sink for auxin below the quiescent center of
the root meristem that is essential for auxin distribution and patterning.
acknowledgement: We thank Petra Tänzler, Michaela Lehnen, and Thomas Steinmann for
technical help. We acknowledge the Arabidopsis Biological Resource Center (Columbus,
OH) and Thomas Altman for providing material. We also gratefully acknowledge the
ADIS service group for DNA sequencing and ZIGIA (Center for Functional Genomics
in Arabidopsis) for the En lines. We are grateful to our colleagues, particularly
Leo Gälweiler, Niko Geldner, Matthias Godde, and Kathrin Schrick for critical reading
of the manuscript. This work was supported by a fellowship of the Deutscher Akademischer
Austauschdienset (J.F.), the Deutsche Forschungsgemeinschaft (Schwerpunktprogramm
Phytohormone), the European Communities Biotechnology Programs, the Fonds der Chemischen
Industrie, and the INCO-Copernicus Program.
article_processing_charge: No
article_type: original
author:
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Eva
full_name: Benková, Eva
id: 38F4F166-F248-11E8-B48F-1D18A9856A87
last_name: Benková
orcid: 0000-0002-8510-9739
- first_name: Ikram
full_name: Blilou, Ikram
last_name: Blilou
- first_name: Justyna
full_name: Wiśniewska, Justyna
last_name: Wiśniewska
- first_name: Thorsten
full_name: Hamann, Thorsten
last_name: Hamann
- first_name: Karin
full_name: Ljung, Karin
last_name: Ljung
- first_name: Scott
full_name: Woody, Scott
last_name: Woody
- first_name: Göran
full_name: Sandberg, Göran
last_name: Sandberg
- first_name: Ben
full_name: Scheres, Ben
last_name: Scheres
- first_name: Gerd
full_name: Jürgens, Gerd
last_name: Jürgens
- first_name: Klaus
full_name: Palme, Klaus
last_name: Palme
citation:
ama: Friml J, Benková E, Blilou I, et al. AtPIN4 mediates sink-driven auxin gradients
and root patterning in Arabidopsis. Cell. 2002;108(5):661-673. doi:10.1016/S0092-8674(02)00656-6
apa: Friml, J., Benková, E., Blilou, I., Wiśniewska, J., Hamann, T., Ljung, K.,
… Palme, K. (2002). AtPIN4 mediates sink-driven auxin gradients and root patterning
in Arabidopsis. Cell. Cell Press. https://doi.org/10.1016/S0092-8674(02)00656-6
chicago: Friml, Jiří, Eva Benková, Ikram Blilou, Justyna Wiśniewska, Thorsten Hamann,
Karin Ljung, Scott Woody, et al. “AtPIN4 Mediates Sink-Driven Auxin Gradients
and Root Patterning in Arabidopsis.” Cell. Cell Press, 2002. https://doi.org/10.1016/S0092-8674(02)00656-6.
ieee: J. Friml et al., “AtPIN4 mediates sink-driven auxin gradients and root
patterning in Arabidopsis,” Cell, vol. 108, no. 5. Cell Press, pp. 661–673,
2002.
ista: Friml J, Benková E, Blilou I, Wiśniewska J, Hamann T, Ljung K, Woody S, Sandberg
G, Scheres B, Jürgens G, Palme K. 2002. AtPIN4 mediates sink-driven auxin gradients
and root patterning in Arabidopsis. Cell. 108(5), 661–673.
mla: Friml, Jiří, et al. “AtPIN4 Mediates Sink-Driven Auxin Gradients and Root Patterning
in Arabidopsis.” Cell, vol. 108, no. 5, Cell Press, 2002, pp. 661–73, doi:10.1016/S0092-8674(02)00656-6.
short: J. Friml, E. Benková, I. Blilou, J. Wiśniewska, T. Hamann, K. Ljung, S. Woody,
G. Sandberg, B. Scheres, G. Jürgens, K. Palme, Cell 108 (2002) 661–673.
date_created: 2018-12-11T12:00:43Z
date_published: 2002-03-08T00:00:00Z
date_updated: 2023-07-17T11:57:40Z
day: '08'
doi: 10.1016/S0092-8674(02)00656-6
extern: '1'
external_id:
pmid:
- '11893337'
intvolume: ' 108'
issue: '5'
language:
- iso: eng
month: '03'
oa_version: None
page: 661 - 673
pmid: 1
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Cell Press
publist_id: '3713'
quality_controlled: '1'
scopus_import: '1'
status: public
title: AtPIN4 mediates sink-driven auxin gradients and root patterning in Arabidopsis
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 108
year: '2002'
...
---
_id: '2991'
abstract:
- lang: eng
text: Polar auxin transport controls multiple aspects of plant development including
differential growth, embryo and root patterning and vascular tissue differentiation.
Identification of proteins involved in this process and availability of new tools
enabling `visualization' of auxin and auxin routes in planta largely contributed
to the significant progress that has recently been made. New data support classical
concepts, but several recent findings are likely to challenge our view on the
mechanism of auxin transport. The aim of this review is to provide a comprehensive
overview of the polar auxin transport field. It starts with classical models resulting
from physiological studies, describes the genetic contributions and discusses
the molecular basis of auxin influx and efflux. Finally, selected questions are
presented in the context of developmental biology, integrating available data
from different fields.
author:
- first_name: Jirí
full_name: Friml, Jirí
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
- first_name: Klaus
full_name: Palme, Klaus
last_name: Palme
citation:
ama: Friml J, Palme K. Polar auxin transport - Old questions and new concepts? Plant
Molecular Biology. 2002;49(3-4):273-284. doi:10.1023/A:1015248926412
apa: Friml, J., & Palme, K. (2002). Polar auxin transport - Old questions and
new concepts? Plant Molecular Biology. Springer. https://doi.org/10.1023/A:1015248926412
chicago: Friml, Jiří, and Klaus Palme. “Polar Auxin Transport - Old Questions and
New Concepts?” Plant Molecular Biology. Springer, 2002. https://doi.org/10.1023/A:1015248926412.
ieee: J. Friml and K. Palme, “Polar auxin transport - Old questions and new concepts?,”
Plant Molecular Biology, vol. 49, no. 3–4. Springer, pp. 273–284, 2002.
ista: Friml J, Palme K. 2002. Polar auxin transport - Old questions and new concepts?
Plant Molecular Biology. 49(3–4), 273–284.
mla: Friml, Jiří, and Klaus Palme. “Polar Auxin Transport - Old Questions and New
Concepts?” Plant Molecular Biology, vol. 49, no. 3–4, Springer, 2002, pp.
273–84, doi:10.1023/A:1015248926412.
short: J. Friml, K. Palme, Plant Molecular Biology 49 (2002) 273–284.
date_created: 2018-12-11T12:00:44Z
date_published: 2002-06-01T00:00:00Z
date_updated: 2021-01-12T07:40:17Z
day: '01'
doi: 10.1023/A:1015248926412
extern: '1'
intvolume: ' 49'
issue: 3-4
language:
- iso: eng
month: '06'
oa_version: None
page: 273 - 284
publication: Plant Molecular Biology
publication_status: published
publisher: Springer
publist_id: '3712'
quality_controlled: '1'
status: public
title: Polar auxin transport - Old questions and new concepts?
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 49
year: '2002'
...
---
_id: '3140'
abstract:
- lang: eng
text: The maturation of synaptic structures depends on inductive interactions between
axons and their prospective targets. One example of such an interaction is the
influence of proprioceptive sensory axons on the differentiation of muscle spindles.
We have monitored the expression of three transcription factors, Egr3, Pea3, and
Erm, that delineate early muscle spindle development in an assay of muscle spindle-inducing
signals. We provide genetic evidence that Neuregulin1 (Nrg1) is required for proprioceptive
afferent-evoked induction of muscle spindle differentiation in the mouse. Ig-Nrg1
isoforms are preferentially expressed by proprioceptive sensory neurons and are
sufficient to induce muscle spindle differentiation in vivo, whereas CRD-Nrg1
isoforms are broadly expressed in sensory and motor neurons but are not required
for muscle spindle induction.
acknowledgement: We thank L. Role for generously providing the CRD-Nrg1 mutant allele
for these studies, L. Parada and D. Anderson for sharing the TrkC and Ngn1 mouse
strains, W. Tourtellotte for providing Egr3 mutant mice, E. Avetisova for expert
technical assistance, X. Yang for experimental help in the initial phase of these
studies, A. Garratt for advice with ErbB antibodies, and L. Role and G. Fischbach
for helpful discussions. The CRD-Nrg1 mutant allele was generated in the lab of
Dr. Lorna Role, with the support of NIH grant NS29071. S.A. and S.H. were supported
by a grant from the Swiss National Science Foundation and the Kanton of Basel-Stadt.
S.J.B. was supported by grants from the NINDS. N.A.S. was supported by a Howard
Hughes Medical Institute Postdoctoral Fellowship for Physicians and a Career Development
Award from the NINDS. T.M.J. was supported by grants from NINDS and is an Investigator
of the Howard Hughes Medical Institute.
article_processing_charge: No
article_type: original
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Neil
full_name: Shneider, Neil
last_name: Shneider
- first_name: Carmen
full_name: Birchmeier, Carmen
last_name: Birchmeier
- first_name: Steven
full_name: Burden, Steven
last_name: Burden
- first_name: Thomas
full_name: Jessell, Thomas
last_name: Jessell
- first_name: Silvia
full_name: Arber, Silvia
last_name: Arber
citation:
ama: Hippenmeyer S, Shneider N, Birchmeier C, Burden S, Jessell T, Arber S. A role
for Neuregulin1 signaling in muscle spindle differentiation. Neuron. 2002;36(6):1035-1049.
doi:10.1016/S0896-6273(02)01101-7
apa: Hippenmeyer, S., Shneider, N., Birchmeier, C., Burden, S., Jessell, T., &
Arber, S. (2002). A role for Neuregulin1 signaling in muscle spindle differentiation.
Neuron. Elsevier. https://doi.org/10.1016/S0896-6273(02)01101-7
chicago: Hippenmeyer, Simon, Neil Shneider, Carmen Birchmeier, Steven Burden, Thomas
Jessell, and Silvia Arber. “A Role for Neuregulin1 Signaling in Muscle Spindle
Differentiation.” Neuron. Elsevier, 2002. https://doi.org/10.1016/S0896-6273(02)01101-7.
ieee: S. Hippenmeyer, N. Shneider, C. Birchmeier, S. Burden, T. Jessell, and S.
Arber, “A role for Neuregulin1 signaling in muscle spindle differentiation,” Neuron,
vol. 36, no. 6. Elsevier, pp. 1035–1049, 2002.
ista: Hippenmeyer S, Shneider N, Birchmeier C, Burden S, Jessell T, Arber S. 2002.
A role for Neuregulin1 signaling in muscle spindle differentiation. Neuron. 36(6),
1035–1049.
mla: Hippenmeyer, Simon, et al. “A Role for Neuregulin1 Signaling in Muscle Spindle
Differentiation.” Neuron, vol. 36, no. 6, Elsevier, 2002, pp. 1035–49,
doi:10.1016/S0896-6273(02)01101-7.
short: S. Hippenmeyer, N. Shneider, C. Birchmeier, S. Burden, T. Jessell, S. Arber,
Neuron 36 (2002) 1035–1049.
date_created: 2018-12-11T12:01:37Z
date_published: 2002-12-19T00:00:00Z
date_updated: 2023-07-17T11:46:43Z
day: '19'
doi: 10.1016/S0896-6273(02)01101-7
extern: '1'
external_id:
pmid:
- '12495620'
intvolume: ' 36'
issue: '6'
language:
- iso: eng
month: '12'
oa_version: None
page: 1035 - 1049
pmid: 1
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
publist_id: '3558'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A role for Neuregulin1 signaling in muscle spindle differentiation
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 36
year: '2002'
...
---
_id: '11123'
abstract:
- lang: eng
text: The small GTPase Ran is a key regulator of nucleocytoplasmic transport during
interphase. The asymmetric distribution of the GTP-bound form of Ran across the
nuclear envelope — that is, large quantities in the nucleus compared with small
quantities in the cytoplasm — determines the directionality of many nuclear transport
processes. Recent findings that Ran also functions in spindle formation and nuclear
envelope assembly during mitosis suggest that Ran has a general role in chromatin-centred
processes. Ran functions in these events as a signal for chromosome position.
article_processing_charge: No
article_type: original
author:
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
- first_name: Oliver J.
full_name: Gruss, Oliver J.
last_name: Gruss
- first_name: Iain W.
full_name: Mattaj, Iain W.
last_name: Mattaj
citation:
ama: Hetzer M, Gruss OJ, Mattaj IW. The Ran GTPase as a marker of chromosome position
in spindle formation and nuclear envelope assembly. Nature Cell Biology.
2002;4(7):E177-E184. doi:10.1038/ncb0702-e177
apa: Hetzer, M., Gruss, O. J., & Mattaj, I. W. (2002). The Ran GTPase as a marker
of chromosome position in spindle formation and nuclear envelope assembly. Nature
Cell Biology. Springer Nature. https://doi.org/10.1038/ncb0702-e177
chicago: Hetzer, Martin, Oliver J. Gruss, and Iain W. Mattaj. “The Ran GTPase as
a Marker of Chromosome Position in Spindle Formation and Nuclear Envelope Assembly.”
Nature Cell Biology. Springer Nature, 2002. https://doi.org/10.1038/ncb0702-e177.
ieee: M. Hetzer, O. J. Gruss, and I. W. Mattaj, “The Ran GTPase as a marker of chromosome
position in spindle formation and nuclear envelope assembly,” Nature Cell Biology,
vol. 4, no. 7. Springer Nature, pp. E177–E184, 2002.
ista: Hetzer M, Gruss OJ, Mattaj IW. 2002. The Ran GTPase as a marker of chromosome
position in spindle formation and nuclear envelope assembly. Nature Cell Biology.
4(7), E177–E184.
mla: Hetzer, Martin, et al. “The Ran GTPase as a Marker of Chromosome Position in
Spindle Formation and Nuclear Envelope Assembly.” Nature Cell Biology,
vol. 4, no. 7, Springer Nature, 2002, pp. E177–84, doi:10.1038/ncb0702-e177.
short: M. Hetzer, O.J. Gruss, I.W. Mattaj, Nature Cell Biology 4 (2002) E177–E184.
date_created: 2022-04-07T07:57:19Z
date_published: 2002-07-01T00:00:00Z
date_updated: 2022-07-18T08:58:03Z
day: '01'
doi: 10.1038/ncb0702-e177
extern: '1'
external_id:
pmid:
- '12105431'
intvolume: ' 4'
issue: '7'
keyword:
- Cell Biology
language:
- iso: eng
month: '07'
oa_version: None
page: E177-E184
pmid: 1
publication: Nature Cell Biology
publication_identifier:
eissn:
- 1476-4679
issn:
- 1465-7392
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Ran GTPase as a marker of chromosome position in spindle formation and
nuclear envelope assembly
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 4
year: '2002'
...
---
_id: '11124'
abstract:
- lang: eng
text: Ran GTPase plays important roles in nucleocytoplasmic transport in interphase
[1, 2] and in both spindle formation and nuclear envelope (NE) assembly during
mitosis [3, 4, 5]. The latter functions rely on the presence of high local concentrations
of GTP-bound Ran near mitotic chromatin [3, 4, 5]. RanGTP localization has been
proposed to result from the association of Ran's GDP/GTP exchange factor, RCC1,
with chromatin [6, 7, 8, 9], but Ran is shown here to bind directly to chromatin
in two modes, either dependent or independent of RCC1, and, where bound, to increase
the affinity of chromatin for NE membranes. We propose that the Ran binding capacity
of chromatin contributes to localized spindle and NE assembly.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Daniel
full_name: Bilbao-Cortés, Daniel
last_name: Bilbao-Cortés
- first_name: Martin W
full_name: HETZER, Martin W
id: 86c0d31b-b4eb-11ec-ac5a-eae7b2e135ed
last_name: HETZER
orcid: 0000-0002-2111-992X
- first_name: Gernot
full_name: Längst, Gernot
last_name: Längst
- first_name: Peter B.
full_name: Becker, Peter B.
last_name: Becker
- first_name: Iain W.
full_name: Mattaj, Iain W.
last_name: Mattaj
citation:
ama: Bilbao-Cortés D, Hetzer M, Längst G, Becker PB, Mattaj IW. Ran binds to chromatin
by two distinct mechanisms. Current Biology. 2002;12(13):1151-1156. doi:10.1016/s0960-9822(02)00927-2
apa: Bilbao-Cortés, D., Hetzer, M., Längst, G., Becker, P. B., & Mattaj, I.
W. (2002). Ran binds to chromatin by two distinct mechanisms. Current Biology.
Elsevier BV. https://doi.org/10.1016/s0960-9822(02)00927-2
chicago: Bilbao-Cortés, Daniel, Martin Hetzer, Gernot Längst, Peter B. Becker, and
Iain W. Mattaj. “Ran Binds to Chromatin by Two Distinct Mechanisms.” Current
Biology. Elsevier BV, 2002. https://doi.org/10.1016/s0960-9822(02)00927-2.
ieee: D. Bilbao-Cortés, M. Hetzer, G. Längst, P. B. Becker, and I. W. Mattaj, “Ran
binds to chromatin by two distinct mechanisms,” Current Biology, vol. 12,
no. 13. Elsevier BV, pp. 1151–1156, 2002.
ista: Bilbao-Cortés D, Hetzer M, Längst G, Becker PB, Mattaj IW. 2002. Ran binds
to chromatin by two distinct mechanisms. Current Biology. 12(13), 1151–1156.
mla: Bilbao-Cortés, Daniel, et al. “Ran Binds to Chromatin by Two Distinct Mechanisms.”
Current Biology, vol. 12, no. 13, Elsevier BV, 2002, pp. 1151–56, doi:10.1016/s0960-9822(02)00927-2.
short: D. Bilbao-Cortés, M. Hetzer, G. Längst, P.B. Becker, I.W. Mattaj, Current
Biology 12 (2002) 1151–1156.
date_created: 2022-04-07T07:57:31Z
date_published: 2002-07-09T00:00:00Z
date_updated: 2022-07-18T08:58:05Z
day: '09'
doi: 10.1016/s0960-9822(02)00927-2
extern: '1'
external_id:
pmid:
- '12121625'
intvolume: ' 12'
issue: '13'
keyword:
- General Agricultural and Biological Sciences
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/S0960-9822(02)00927-2
month: '07'
oa: 1
oa_version: Published Version
page: 1151-1156
pmid: 1
publication: Current Biology
publication_identifier:
issn:
- 0960-9822
publication_status: published
publisher: Elsevier BV
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ran binds to chromatin by two distinct mechanisms
type: journal_article
user_id: 72615eeb-f1f3-11ec-aa25-d4573ddc34fd
volume: 12
year: '2002'
...
---
_id: '859'
abstract:
- lang: eng
text: The polymeric ubiquitin (poly-u) genes are composed of tandem 228-bp repeats
with no spacer sequences between individual monomer units. Ubiquitin is one of
the most conserved proteins known to date, and the individual units within a number
of poly-u genes are significantly more similar to each other than would be expected
if each unit evolved independently. It has been proposed that the rather striking
similarity among poly-u monomers in some lineages is caused by a series of homogenization
events. Here we report the sequences of the polyubiquitin-C (Ubc) genes in two
mouse strains. Analysis of these sequences, as well as those of the previously
reported Chinese hamster and rat poly-u genes, supports the assertion that the
homogenization of the ubiquitin-C gene in rodents is due to unequal crossing-over
events. The sequence divergence of noncoding DNA was used to estimate the frequency
of unequal crossing-over events (6.3 x 10-5 events per generation) in the Ubc
gene, as well as to provide evidence of apparent selection in the poly-u gene.
acknowledgement: We are thankful to J.A. Southerland and P.L. Jiang for technical
assistance in DNA sequencing, as well as to Y.I. Pavlov for helpful discussions.
This work was supported by public Health Service Research Grant AI45135 from the
Institute of Allergy and Infectious Diseases, National Institutes of Health.
article_processing_charge: No
article_type: original
author:
- first_name: Andrey
full_name: Perelygin, Andrey
last_name: Perelygin
- first_name: Fyodor
full_name: Kondrashov, Fyodor
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
- first_name: Igor
full_name: Rogozin, Igor
last_name: Rogozin
- first_name: Margo
full_name: Brinton, Margo
last_name: Brinton
citation:
ama: Perelygin A, Kondrashov F, Rogozin I, Brinton M. Evolution of the mouse polyubiquitin
C gene. Journal of Molecular Evolution. 2002;55(2):202-210. doi:10.1007/s00239-002-2318-0
apa: Perelygin, A., Kondrashov, F., Rogozin, I., & Brinton, M. (2002). Evolution
of the mouse polyubiquitin C gene. Journal of Molecular Evolution. Springer.
https://doi.org/10.1007/s00239-002-2318-0
chicago: Perelygin, Andrey, Fyodor Kondrashov, Igor Rogozin, and Margo Brinton.
“Evolution of the Mouse Polyubiquitin C Gene.” Journal of Molecular Evolution.
Springer, 2002. https://doi.org/10.1007/s00239-002-2318-0.
ieee: A. Perelygin, F. Kondrashov, I. Rogozin, and M. Brinton, “Evolution of the
mouse polyubiquitin C gene,” Journal of Molecular Evolution, vol. 55, no.
2. Springer, pp. 202–210, 2002.
ista: Perelygin A, Kondrashov F, Rogozin I, Brinton M. 2002. Evolution of the mouse
polyubiquitin C gene. Journal of Molecular Evolution. 55(2), 202–210.
mla: Perelygin, Andrey, et al. “Evolution of the Mouse Polyubiquitin C Gene.” Journal
of Molecular Evolution, vol. 55, no. 2, Springer, 2002, pp. 202–10, doi:10.1007/s00239-002-2318-0.
short: A. Perelygin, F. Kondrashov, I. Rogozin, M. Brinton, Journal of Molecular
Evolution 55 (2002) 202–210.
date_created: 2018-12-11T11:48:53Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-26T12:01:34Z
day: '01'
doi: 10.1007/s00239-002-2318-0
extern: '1'
external_id:
pmid:
- '12107596'
intvolume: ' 55'
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 202 - 210
pmid: 1
publication: Journal of Molecular Evolution
publication_identifier:
issn:
- 0022-2844
publication_status: published
publisher: Springer
publist_id: '6787'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Evolution of the mouse polyubiquitin C gene
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 55
year: '2002'
...
---
_id: '871'
abstract:
- lang: eng
text: 'BACKGROUND: Gene duplications have a major role in the evolution of new biological
functions. Theoretical studies often assume that a duplication per se is selectively
neutral and that, following a duplication, one of the gene copies is freed from
purifying (stabilizing) selection, which creates the potential for evolution of
a new function. RESULTS: In search of systematic evidence of accelerated evolution
after duplication, we used data from 26 bacterial, six archaeal, and seven eukaryotic
genomes to compare the mode and strength of selection acting on recently duplicated
genes (paralogs) and on similarly diverged, unduplicated orthologous genes in
different species. We find that the ratio of nonsynonymous to synonymous substitutions
(Kn/Ks) in most paralogous pairs is <<1 and that paralogs typically evolve
at similar rates, without significant asymmetry, indicating that both paralogs
produced by a duplication are subject to purifying selection. This selection is,
however, substantially weaker than the purifying selection affecting unduplicated
orthologs that have diverged to the same extent as the analyzed paralogs. Most
of the recently duplicated genes appear to be involved in various forms of environmental
response; in particular, many of them encode membrane and secreted proteins. CONCLUSIONS:
The results of this analysis indicate that recently duplicated paralogs evolve
faster than orthologs with the same level of divergence and similar functions,
but apparently do not experience a phase of neutral evolution. We hypothesize
that gene duplications that persist in an evolving lineage are beneficial from
the time of their origin, due primarily to a protein dosage effect in response
to variable environmental conditions; duplications are likely to give rise to
new functions at a later phase of their evolution once a higher level of divergence
is reached.'
acknowledgement: We are grateful to A.S. Kondrashov for numerous helpful suggestions,
to I. King Jordan, M.A. Roytberg, J.L. Spouge and D.A. Kondrashov for useful discussions
and to A.S. Kondrashov, I. King Jordan and D.J. Lipman for critical reading of the
manuscript.
article_processing_charge: No
article_type: original
author:
- first_name: Fyodor
full_name: Kondrashov, Fyodor
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
- first_name: Igor
full_name: Rogozin, Igor
last_name: Rogozin
- first_name: Yuri
full_name: Wolf, Yuri
last_name: Wolf
- first_name: Eugene
full_name: Koonin, Eugene
last_name: Koonin
citation:
ama: Kondrashov F, Rogozin I, Wolf Y, Koonin E. Selection in the evolution of gene
duplications . Genome Biology. 2002;3(2). doi:10.1186/gb-2002-3-2-research0008
apa: Kondrashov, F., Rogozin, I., Wolf, Y., & Koonin, E. (2002). Selection in
the evolution of gene duplications . Genome Biology. BioMed Central. https://doi.org/10.1186/gb-2002-3-2-research0008
chicago: Kondrashov, Fyodor, Igor Rogozin, Yuri Wolf, and Eugene Koonin. “Selection
in the Evolution of Gene Duplications .” Genome Biology. BioMed Central,
2002. https://doi.org/10.1186/gb-2002-3-2-research0008.
ieee: F. Kondrashov, I. Rogozin, Y. Wolf, and E. Koonin, “Selection in the evolution
of gene duplications ,” Genome Biology, vol. 3, no. 2. BioMed Central,
2002.
ista: Kondrashov F, Rogozin I, Wolf Y, Koonin E. 2002. Selection in the evolution
of gene duplications . Genome Biology. 3(2).
mla: Kondrashov, Fyodor, et al. “Selection in the Evolution of Gene Duplications
.” Genome Biology, vol. 3, no. 2, BioMed Central, 2002, doi:10.1186/gb-2002-3-2-research0008.
short: F. Kondrashov, I. Rogozin, Y. Wolf, E. Koonin, Genome Biology 3 (2002).
date_created: 2018-12-11T11:48:57Z
date_published: 2002-01-01T00:00:00Z
date_updated: 2023-07-26T11:48:27Z
day: '01'
doi: 10.1186/gb-2002-3-2-research0008
extern: '1'
external_id:
pmid:
- '11864370'
intvolume: ' 3'
issue: '2'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC65685/
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
publication: Genome Biology
publication_identifier:
issn:
- 1465-6906
publication_status: published
publisher: BioMed Central
publist_id: '6781'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Selection in the evolution of gene duplications '
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 3
year: '2002'
...
---
_id: '885'
abstract:
- lang: eng
text: We study fitness landscape in the space of protein sequences by relating sets
of human pathogenic missense mutations in 32 proteins to amino acid substitutions
that occurred in the course of evolution of these proteins. On average, ≈10% of
deviations of a nonhuman protein from its human ortholog are compensated pathogenic
deviations (CPDs), i.e., are caused by an amino acid substitution that, at this
site, would be pathogenic to humans. Normal functioning of a CPD-containing protein
must be caused by other, compensatory deviations of the nonhuman species from
humans. Together, a CPD and the corresponding compensatory deviation form a Dobzhansky-Muller
incompatibility that can be visualized as the corner on a fitness ridge. Thus,
proteins evolve along fitness ridges which contain only ≈10 steps between sucessive
corners. The fraction of CPDs among all deviations of a protein from its human
ortholog does not increase with the evolutionary distance between the proteins,
indicating that subtitutions that carry evolving proteins around these corners
occur in rapid succession, driven by positive selection. Data on fitness of interspecies
hybrids suggest that the compensatory change that makes a CPD fit usually occurs
within the same protein. Data on protein structures and on cooccurrence of amino
acids at different sites of multiple orthologous proteins often make it possible
to provisionally identify the substitution that compensates a partiCUlar CPD.
article_processing_charge: No
article_type: original
author:
- first_name: Alexey
full_name: Kondrashov, Alexey
last_name: Kondrashov
- first_name: Shamil
full_name: Sunyaev, Shamil
last_name: Sunyaev
- first_name: Fyodor
full_name: Kondrashov, Fyodor
id: 44FDEF62-F248-11E8-B48F-1D18A9856A87
last_name: Kondrashov
orcid: 0000-0001-8243-4694
citation:
ama: Kondrashov A, Sunyaev S, Kondrashov F. Dobzhansky-Muller incompatibilities
in protein evolution. PNAS. 2002;99(23):14878-14883. doi:10.1073/pnas.232565499
apa: Kondrashov, A., Sunyaev, S., & Kondrashov, F. (2002). Dobzhansky-Muller
incompatibilities in protein evolution. PNAS. National Academy of Sciences.
https://doi.org/10.1073/pnas.232565499
chicago: Kondrashov, Alexey, Shamil Sunyaev, and Fyodor Kondrashov. “Dobzhansky-Muller
Incompatibilities in Protein Evolution.” PNAS. National Academy of Sciences,
2002. https://doi.org/10.1073/pnas.232565499.
ieee: A. Kondrashov, S. Sunyaev, and F. Kondrashov, “Dobzhansky-Muller incompatibilities
in protein evolution,” PNAS, vol. 99, no. 23. National Academy of Sciences,
pp. 14878–14883, 2002.
ista: Kondrashov A, Sunyaev S, Kondrashov F. 2002. Dobzhansky-Muller incompatibilities
in protein evolution. PNAS. 99(23), 14878–14883.
mla: Kondrashov, Alexey, et al. “Dobzhansky-Muller Incompatibilities in Protein
Evolution.” PNAS, vol. 99, no. 23, National Academy of Sciences, 2002,
pp. 14878–83, doi:10.1073/pnas.232565499.
short: A. Kondrashov, S. Sunyaev, F. Kondrashov, PNAS 99 (2002) 14878–14883.
date_created: 2018-12-11T11:49:01Z
date_published: 2002-11-12T00:00:00Z
date_updated: 2023-07-26T09:48:37Z
day: '12'
doi: 10.1073/pnas.232565499
extern: '1'
external_id:
pmid:
- '12403824'
intvolume: ' 99'
issue: '23'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC137512/
month: '11'
oa: 1
oa_version: Published Version
page: 14878 - 14883
pmid: 1
publication: PNAS
publication_identifier:
issn:
- 0027-8424
publication_status: published
publisher: National Academy of Sciences
publist_id: '6763'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dobzhansky-Muller incompatibilities in protein evolution
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 99
year: '2002'
...