---
_id: '3132'
abstract:
- lang: eng
text: 'Reproductive division of labour is a characteristic trait of social insects.
The dominant reproductive individual, often the queen, uses chemical communication
and/or behaviour to maintain her social status. Queens of many social insects
communicate their fertility status via cuticle-bound substances. As these substances
usually possess a low volatility, their range in queen–worker communication is
potentially limited. Here, we investigate the range and impact of behavioural
and chemical queen signals on workers of the ant Temnothorax longispinosus. We
compared the behaviour and ovary development of workers subjected to three different
treatments: workers with direct chemical and physical contact to the queen, those
solely under the influence of volatile queen substances and those entirely separated
from the queen. In addition to short-ranged queen signals preventing ovary development
in workers, we discovered a novel secondary pathway influencing worker behaviour.
Workers with no physical contact to the queen, but exposed to volatile substances,
started to develop their ovaries, but did not change their behaviour compared
to workers in direct contact to the queen. In contrast, workers in queen-separated
groups showed both increased ovary development and aggressive dominance interactions.
We conclude that T. longispinosus queens influence worker ovary development and
behaviour via two independent signals, both ensuring social harmony within the
colony.'
acknowledgement: We like to thank the editor and three anonymous reviewers for their
time and constructive criticism and Inon Scharf, Volker Witte and Andreas Modlmeier
for helpful comments on earlier versions of the manuscript. The first and second
authors appear in alphabetical order and contributed equally to this paper.
author:
- first_name: Matthias
full_name: Konrad, Matthias
id: 46528076-F248-11E8-B48F-1D18A9856A87
last_name: Konrad
- first_name: Tobias
full_name: Pamminger, Tobias
last_name: Pamminger
- first_name: Susanne
full_name: Foitzik, Susanne
last_name: Foitzik
citation:
ama: Konrad M, Pamminger T, Foitzik S. Two pathways ensuring social harmony. Naturwissenschaften.
2012;99(8):627-636. doi:10.1007/s00114-012-0943-z
apa: Konrad, M., Pamminger, T., & Foitzik, S. (2012). Two pathways ensuring
social harmony. Naturwissenschaften. Springer. https://doi.org/10.1007/s00114-012-0943-z
chicago: Konrad, Matthias, Tobias Pamminger, and Susanne Foitzik. “Two Pathways
Ensuring Social Harmony.” Naturwissenschaften. Springer, 2012. https://doi.org/10.1007/s00114-012-0943-z.
ieee: M. Konrad, T. Pamminger, and S. Foitzik, “Two pathways ensuring social harmony,”
Naturwissenschaften, vol. 99, no. 8. Springer, pp. 627–636, 2012.
ista: Konrad M, Pamminger T, Foitzik S. 2012. Two pathways ensuring social harmony.
Naturwissenschaften. 99(8), 627–636.
mla: Konrad, Matthias, et al. “Two Pathways Ensuring Social Harmony.” Naturwissenschaften,
vol. 99, no. 8, Springer, 2012, pp. 627–36, doi:10.1007/s00114-012-0943-z.
short: M. Konrad, T. Pamminger, S. Foitzik, Naturwissenschaften 99 (2012) 627–636.
date_created: 2018-12-11T12:01:34Z
date_published: 2012-08-01T00:00:00Z
date_updated: 2021-01-12T07:41:17Z
day: '01'
department:
- _id: SyCr
doi: 10.1007/s00114-012-0943-z
intvolume: ' 99'
issue: '8'
language:
- iso: eng
month: '08'
oa_version: None
page: 627 - 636
publication: Naturwissenschaften
publication_status: published
publisher: Springer
publist_id: '3565'
quality_controlled: '1'
scopus_import: 1
status: public
title: Two pathways ensuring social harmony
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 99
year: '2012'
...
---
_id: '3161'
abstract:
- lang: eng
text: 'Some inflammatory stimuli trigger activation of the NLRP3 inflammasome by
inducing efflux of cellular potassium. Loss of cellular potassium is known to
potently suppress protein synthesis, leading us to test whether the inhibition
of protein synthesis itself serves as an activating signal for the NLRP3 inflammasome.
Murine bone marrow-derived macrophages, either primed by LPS or unprimed, were
exposed to a panel of inhibitors of ribosomal function: ricin, cycloheximide,
puromycin, pactamycin, and anisomycin. Macrophages were also exposed to nigericin,
ATP, monosodium urate (MSU), and poly I:C. Synthesis of pro-IL-ß and release of
IL-1ß from cells in response to these agents was detected by immunoblotting and
ELISA. Release of intracellular potassium was measured by mass spectrometry. Inhibition
of translation by each of the tested translation inhibitors led to processing
of IL-1ß, which was released from cells. Processing and release of IL-1ß was reduced
or absent from cells deficient in NLRP3, ASC, or caspase-1, demonstrating the
role of the NLRP3 inflammasome. Despite the inability of these inhibitors to trigger
efflux of intracellular potassium, the addition of high extracellular potassium
suppressed activation of the NLRP3 inflammasome. MSU and double-stranded RNA,
which are known to activate the NLRP3 inflammasome, also substantially inhibited
protein translation, supporting a close association between inhibition of translation
and inflammasome activation. These data demonstrate that translational inhibition
itself constitutes a heretofore-unrecognized mechanism underlying IL-1ß dependent
inflammatory signaling and that other physical, chemical, or pathogen-associated
agents that impair translation may lead to IL-1ß-dependent inflammation through
activation of the NLRP3 inflammasome. For agents that inhibit translation through
decreased cellular potassium, the application of high extracellular potassium
restores protein translation and suppresses activation of the NLRP inflammasome.
For agents that inhibit translation through mechanisms that do not involve loss
of potassium, high extracellular potassium suppresses IL-1ß processing through
a mechanism that remains undefined.'
acknowledgement: "Supported by National Institutes of Health grants GM071338 (ML)
and AI059355 (BM).\r\nWe acknowledge the expertise of Dr. Martina Ralle in Department
of Biochemistry and Molecular Biology at OHSU for measurements of potassium using
inductively coupled plasma mass spectrometry."
article_number: e36044
author:
- first_name: Meghan
full_name: Vyleta, Meghan
id: 418901AA-F248-11E8-B48F-1D18A9856A87
last_name: Vyleta
- first_name: John
full_name: Wong, John
last_name: Wong
- first_name: Bruce
full_name: Magun, Bruce
last_name: Magun
citation:
ama: Vyleta M, Wong J, Magun B. Suppression of ribosomal function triggers innate
immune signaling through activation of the NLRP3 inflammasome. PLoS One.
2012;7(5). doi:10.1371/journal.pone.0036044
apa: Vyleta, M., Wong, J., & Magun, B. (2012). Suppression of ribosomal function
triggers innate immune signaling through activation of the NLRP3 inflammasome.
PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0036044
chicago: Vyleta, Meghan, John Wong, and Bruce Magun. “Suppression of Ribosomal Function
Triggers Innate Immune Signaling through Activation of the NLRP3 Inflammasome.”
PLoS One. Public Library of Science, 2012. https://doi.org/10.1371/journal.pone.0036044.
ieee: M. Vyleta, J. Wong, and B. Magun, “Suppression of ribosomal function triggers
innate immune signaling through activation of the NLRP3 inflammasome,” PLoS
One, vol. 7, no. 5. Public Library of Science, 2012.
ista: Vyleta M, Wong J, Magun B. 2012. Suppression of ribosomal function triggers
innate immune signaling through activation of the NLRP3 inflammasome. PLoS One.
7(5), e36044.
mla: Vyleta, Meghan, et al. “Suppression of Ribosomal Function Triggers Innate Immune
Signaling through Activation of the NLRP3 Inflammasome.” PLoS One, vol.
7, no. 5, e36044, Public Library of Science, 2012, doi:10.1371/journal.pone.0036044.
short: M. Vyleta, J. Wong, B. Magun, PLoS One 7 (2012).
date_created: 2018-12-11T12:01:45Z
date_published: 2012-05-14T00:00:00Z
date_updated: 2021-01-12T07:41:29Z
day: '14'
ddc:
- '610'
department:
- _id: SyCr
doi: 10.1371/journal.pone.0036044
file:
- access_level: open_access
checksum: 30cef37e27eaa467f6571b3640282010
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:30Z
date_updated: 2020-07-14T12:46:01Z
file_id: '5082'
file_name: IST-2012-97-v1+1_journal.pone.0036044.pdf
file_size: 2984012
relation: main_file
file_date_updated: 2020-07-14T12:46:01Z
has_accepted_license: '1'
intvolume: ' 7'
issue: '5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '3526'
pubrep_id: '97'
quality_controlled: '1'
scopus_import: 1
status: public
title: Suppression of ribosomal function triggers innate immune signaling through
activation of the NLRP3 inflammasome
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 7
year: '2012'
...
---
_id: '3162'
abstract:
- lang: eng
text: Given a dense-time real-valued signal and a parameterized temporal logic formula
with both magnitude and timing parameters, we compute the subset of the parameter
space that renders the formula satisfied by the trace. We provide two preliminary
implementations, one which follows the exact semantics and attempts to compute
the validity domain by quantifier elimination in linear arithmetics and one which
conducts adaptive search in the parameter space.
alternative_title:
- LNCS
article_processing_charge: No
author:
- first_name: Eugene
full_name: Asarin, Eugene
last_name: Asarin
- first_name: Alexandre
full_name: Donzé, Alexandre
last_name: Donzé
- first_name: Oded
full_name: Maler, Oded
last_name: Maler
- first_name: Dejan
full_name: Nickovic, Dejan
id: 41BCEE5C-F248-11E8-B48F-1D18A9856A87
last_name: Nickovic
citation:
ama: 'Asarin E, Donzé A, Maler O, Nickovic D. Parametric identification of temporal
properties. In: Vol 7186. Springer; 2012:147-160. doi:10.1007/978-3-642-29860-8_12'
apa: 'Asarin, E., Donzé, A., Maler, O., & Nickovic, D. (2012). Parametric identification
of temporal properties (Vol. 7186, pp. 147–160). Presented at the RV: Runtime
Verification, San Francisco, CA, United States: Springer. https://doi.org/10.1007/978-3-642-29860-8_12'
chicago: Asarin, Eugene, Alexandre Donzé, Oded Maler, and Dejan Nickovic. “Parametric
Identification of Temporal Properties,” 7186:147–60. Springer, 2012. https://doi.org/10.1007/978-3-642-29860-8_12.
ieee: 'E. Asarin, A. Donzé, O. Maler, and D. Nickovic, “Parametric identification
of temporal properties,” presented at the RV: Runtime Verification, San Francisco,
CA, United States, 2012, vol. 7186, pp. 147–160.'
ista: 'Asarin E, Donzé A, Maler O, Nickovic D. 2012. Parametric identification of
temporal properties. RV: Runtime Verification, LNCS, vol. 7186, 147–160.'
mla: Asarin, Eugene, et al. Parametric Identification of Temporal Properties.
Vol. 7186, Springer, 2012, pp. 147–60, doi:10.1007/978-3-642-29860-8_12.
short: E. Asarin, A. Donzé, O. Maler, D. Nickovic, in:, Springer, 2012, pp. 147–160.
conference:
end_date: 2011-09-30
location: San Francisco, CA, United States
name: 'RV: Runtime Verification'
start_date: 2011-09-27
date_created: 2018-12-11T12:01:45Z
date_published: 2012-01-01T00:00:00Z
date_updated: 2021-01-12T07:41:29Z
day: '01'
ddc:
- '000'
department:
- _id: ToHe
doi: 10.1007/978-3-642-29860-8_12
file:
- access_level: open_access
checksum: ba4a75287008fc64b8fbf78a7476ec32
content_type: application/pdf
creator: dernst
date_created: 2020-05-15T12:50:15Z
date_updated: 2020-07-14T12:46:01Z
file_id: '7862'
file_name: 2012_RV_Asarin.pdf
file_size: 374726
relation: main_file
file_date_updated: 2020-07-14T12:46:01Z
has_accepted_license: '1'
intvolume: ' 7186'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Submitted Version
page: 147 - 160
publication_status: published
publisher: Springer
publist_id: '3525'
quality_controlled: '1'
scopus_import: 1
status: public
title: Parametric identification of temporal properties
type: conference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 7186
year: '2012'
...
---
_id: '3160'
abstract:
- lang: eng
text: There is a long-running controversy about how early cell fate decisions are
made in the developing mammalian embryo. 1,2 In particular, it is controversial
when the first events that can predict the establishment of the pluripotent and
extra-embryonic lineages in the blastocyst of the pre-implantation embryo occur.
It has long been proposed that the position and polarity of cells at the 16- to
32-cell stage embryo influence their decision to either give rise to the pluripotent
cell lineage that eventually contributes to the inner cell mass (ICM), comprising
the primitive endoderm (PE) and the epiblast (EPI), or the extra-embryonic trophectoderm
(TE) surrounding the blastocoel. The positioning of cells in the embryo at this
developmental stage could largely be the result of random events, making this
a stochastic model of cell lineage allocation. Contrary to such a stochastic model,
some studies have detected putative differences in the lineage potential of individual
blastomeres before compaction, indicating that the first cell fate decisions may
occur as early as at the 4-cell stage. Using a non-invasive, quantitative in vivo
imaging assay to study the kinetic behavior of Oct4 (also known as POU5F1), a
key transcription factor (TF) controlling pre-implantation development in the
mouse embryo, 3-5 a recent study identifies Oct4 kinetics as a predictive measure
of cell lineage patterning in the early mouse embryo. 6 Here, we discuss the implications
of such molecular heterogeneities in early development and offer potential avenues
toward a mechanistic understanding of these observations, contributing to the
resolution of the controversy of developmental cell lineage allocation.
author:
- first_name: Periklis
full_name: Pantazis, Periklis
last_name: Pantazis
- first_name: Tobias
full_name: Bollenbach, Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
citation:
ama: Pantazis P, Bollenbach MT. Transcription factor kinetics and the emerging asymmetry
in the early mammalian embryo. Cell Cycle. 2012;11(11):2055-2058. doi:10.4161/cc.20118
apa: Pantazis, P., & Bollenbach, M. T. (2012). Transcription factor kinetics
and the emerging asymmetry in the early mammalian embryo. Cell Cycle. Taylor
and Francis. https://doi.org/10.4161/cc.20118
chicago: Pantazis, Periklis, and Mark Tobias Bollenbach. “Transcription Factor Kinetics
and the Emerging Asymmetry in the Early Mammalian Embryo.” Cell Cycle.
Taylor and Francis, 2012. https://doi.org/10.4161/cc.20118.
ieee: P. Pantazis and M. T. Bollenbach, “Transcription factor kinetics and the emerging
asymmetry in the early mammalian embryo,” Cell Cycle, vol. 11, no. 11.
Taylor and Francis, pp. 2055–2058, 2012.
ista: Pantazis P, Bollenbach MT. 2012. Transcription factor kinetics and the emerging
asymmetry in the early mammalian embryo. Cell Cycle. 11(11), 2055–2058.
mla: Pantazis, Periklis, and Mark Tobias Bollenbach. “Transcription Factor Kinetics
and the Emerging Asymmetry in the Early Mammalian Embryo.” Cell Cycle,
vol. 11, no. 11, Taylor and Francis, 2012, pp. 2055–58, doi:10.4161/cc.20118.
short: P. Pantazis, M.T. Bollenbach, Cell Cycle 11 (2012) 2055–2058.
date_created: 2018-12-11T12:01:44Z
date_published: 2012-06-01T00:00:00Z
date_updated: 2021-01-12T07:41:28Z
day: '01'
department:
- _id: ToBo
doi: 10.4161/cc.20118
intvolume: ' 11'
issue: '11'
language:
- iso: eng
month: '06'
oa_version: None
page: 2055 - 2058
publication: Cell Cycle
publication_status: published
publisher: Taylor and Francis
publist_id: '3531'
quality_controlled: '1'
scopus_import: 1
status: public
title: Transcription factor kinetics and the emerging asymmetry in the early mammalian
embryo
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 11
year: '2012'
...
---
_id: '3164'
abstract:
- lang: eng
text: Overview of the Special Issue on structured prediction and inference.
author:
- first_name: Matthew
full_name: Blaschko, Matthew
last_name: Blaschko
- first_name: Christoph
full_name: Lampert, Christoph
id: 40C20FD2-F248-11E8-B48F-1D18A9856A87
last_name: Lampert
orcid: 0000-0001-8622-7887
citation:
ama: 'Blaschko M, Lampert C. Guest editorial: Special issue on structured prediction
and inference. International Journal of Computer Vision. 2012;99(3):257-258.
doi:10.1007/s11263-012-0530-y'
apa: 'Blaschko, M., & Lampert, C. (2012). Guest editorial: Special issue on
structured prediction and inference. International Journal of Computer Vision.
Springer. https://doi.org/10.1007/s11263-012-0530-y'
chicago: 'Blaschko, Matthew, and Christoph Lampert. “Guest Editorial: Special Issue
on Structured Prediction and Inference.” International Journal of Computer
Vision. Springer, 2012. https://doi.org/10.1007/s11263-012-0530-y.'
ieee: 'M. Blaschko and C. Lampert, “Guest editorial: Special issue on structured
prediction and inference,” International Journal of Computer Vision, vol.
99, no. 3. Springer, pp. 257–258, 2012.'
ista: 'Blaschko M, Lampert C. 2012. Guest editorial: Special issue on structured
prediction and inference. International Journal of Computer Vision. 99(3), 257–258.'
mla: 'Blaschko, Matthew, and Christoph Lampert. “Guest Editorial: Special Issue
on Structured Prediction and Inference.” International Journal of Computer
Vision, vol. 99, no. 3, Springer, 2012, pp. 257–58, doi:10.1007/s11263-012-0530-y.'
short: M. Blaschko, C. Lampert, International Journal of Computer Vision 99 (2012)
257–258.
date_created: 2018-12-11T12:01:46Z
date_published: 2012-09-01T00:00:00Z
date_updated: 2021-01-12T07:41:30Z
day: '01'
department:
- _id: ChLa
doi: 10.1007/s11263-012-0530-y
intvolume: ' 99'
issue: '3'
language:
- iso: eng
month: '09'
oa_version: None
page: 257 - 258
publication: International Journal of Computer Vision
publication_status: published
publisher: Springer
publist_id: '3521'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Guest editorial: Special issue on structured prediction and inference'
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 99
year: '2012'
...