---
_id: '8'
abstract:
- lang: eng
text: Despite their different origins, Drosophila glia and hemocytes are related
cell populations that provide an immune function. Drosophila hemocytes patrol
the body cavity and act as macrophages outside the nervous system whereas glia
originate from the neuroepithelium and provide the scavenger population of the
nervous system. Drosophila glia are hence the functional orthologs of vertebrate
microglia, even though the latter are cells of immune origin that subsequently
move into the brain during development. Interestingly, the Drosophila immune cells
within (glia) and outside the nervous system (hemocytes) require the same transcription
factor Glide/Gcm for their development. This raises the issue of how do glia specifically
differentiate in the nervous system and hemocytes in the procephalic mesoderm.
The Repo homeodomain transcription factor and pan-glial direct target of Glide/Gcm
is known to ensure glial terminal differentiation. Here we show that Repo also
takes center stage in the process that discriminates between glia and hemocytes.
First, Repo expression is repressed in the hemocyte anlagen by mesoderm-specific
factors. Second, Repo ectopic activation in the procephalic mesoderm is sufficient
to repress the expression of hemocyte-specific genes. Third, the lack of Repo
triggers the expression of hemocyte markers in glia. Thus, a complex network of
tissue-specific cues biases the potential of Glide/Gcm. These data allow us to
revise the concept of fate determinants and help us understand the bases of cell
specification. Both sexes were analyzed.SIGNIFICANCE STATEMENTDistinct cell types
often require the same pioneer transcription factor, raising the issue of how
does one factor trigger different fates. In Drosophila, glia and hemocytes provide
a scavenger activity within and outside the nervous system, respectively. While
they both require the Glide/Gcm transcription factor, glia originate from the
ectoderm, hemocytes from the mesoderm. Here we show that tissue-specific factors
inhibit the gliogenic potential of Glide/Gcm in the mesoderm by repressing the
expression of the homeodomain protein Repo, a major glial-specific target of Glide/Gcm.
Repo expression in turn inhibits the expression of hemocyte-specific genes in
the nervous system. These cell-specific networks secure the establishment of the
glial fate only in the nervous system and allow cell diversification.
acknowledgement: This work was supported by INSERM, CNRS, UDS, Ligue Régionale contre
le Cancer, Hôpital de Strasbourg, Association pour la Recherche sur le Cancer (ARC)
and Agence Nationale de la Recherche (ANR) grants. P.B.C. was funded by the ANR
and by the ARSEP (Fondation pour l'Aide à la Recherche sur la Sclérose en Plaques),
and G.T. by governmental and ARC fellowships. This work was also supported by grants
from the Ataxia UK (2491) and the NC3R (NC/L000199/1) awarded to M.F. The Institut
de Génétique et de Biologie Moléculaire et Cellulaire was also supported by a French
state fund through the ANR labex. D.E.S. was funded by Marie Curie Grant CIG 334077/IRTIM.
We thank B. Altenhein, K. Brückner, M. Crozatier, L. Waltzer, M. Logan, E. Kurant,
R. Reuter, E. Kurucz, J.L Dimarcq, J. Hoffmann, C. Goodman, the DHSB, and the BDSC
for reagents and flies. We also thank all of the laboratory members for comments
on the manuscript; C. Diebold, C. Delaporte, M. Pezze, the fly, and imaging and
antibody facilities for technical assistance; and D. Dembele for help with statistics.
In addition, we thank Alison Brewer for help with Luciferase assays.
article_processing_charge: No
article_type: original
author:
- first_name: Guillaume
full_name: Trébuchet, Guillaume
last_name: Trébuchet
- first_name: Pierre B
full_name: Cattenoz, Pierre B
last_name: Cattenoz
- first_name: János
full_name: Zsámboki, János
last_name: Zsámboki
- first_name: David
full_name: Mazaud, David
last_name: Mazaud
- first_name: Daria E
full_name: Siekhaus, Daria E
id: 3D224B9E-F248-11E8-B48F-1D18A9856A87
last_name: Siekhaus
orcid: 0000-0001-8323-8353
- first_name: Manolis
full_name: Fanto, Manolis
last_name: Fanto
- first_name: Angela
full_name: Giangrande, Angela
last_name: Giangrande
citation:
ama: Trébuchet G, Cattenoz PB, Zsámboki J, et al. The Repo homeodomain transcription
factor suppresses hematopoiesis in Drosophila and preserves the glial fate. Journal
of Neuroscience. 2019;39(2):238-255. doi:10.1523/JNEUROSCI.1059-18.2018
apa: Trébuchet, G., Cattenoz, P. B., Zsámboki, J., Mazaud, D., Siekhaus, D. E.,
Fanto, M., & Giangrande, A. (2019). The Repo homeodomain transcription factor
suppresses hematopoiesis in Drosophila and preserves the glial fate. Journal
of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1059-18.2018
chicago: Trébuchet, Guillaume, Pierre B Cattenoz, János Zsámboki, David Mazaud,
Daria E Siekhaus, Manolis Fanto, and Angela Giangrande. “The Repo Homeodomain
Transcription Factor Suppresses Hematopoiesis in Drosophila and Preserves the
Glial Fate.” Journal of Neuroscience. Society for Neuroscience, 2019. https://doi.org/10.1523/JNEUROSCI.1059-18.2018.
ieee: G. Trébuchet et al., “The Repo homeodomain transcription factor suppresses
hematopoiesis in Drosophila and preserves the glial fate,” Journal of Neuroscience,
vol. 39, no. 2. Society for Neuroscience, pp. 238–255, 2019.
ista: Trébuchet G, Cattenoz PB, Zsámboki J, Mazaud D, Siekhaus DE, Fanto M, Giangrande
A. 2019. The Repo homeodomain transcription factor suppresses hematopoiesis in
Drosophila and preserves the glial fate. Journal of Neuroscience. 39(2), 238–255.
mla: Trébuchet, Guillaume, et al. “The Repo Homeodomain Transcription Factor Suppresses
Hematopoiesis in Drosophila and Preserves the Glial Fate.” Journal of Neuroscience,
vol. 39, no. 2, Society for Neuroscience, 2019, pp. 238–55, doi:10.1523/JNEUROSCI.1059-18.2018.
short: G. Trébuchet, P.B. Cattenoz, J. Zsámboki, D. Mazaud, D.E. Siekhaus, M. Fanto,
A. Giangrande, Journal of Neuroscience 39 (2019) 238–255.
date_created: 2018-12-11T11:44:07Z
date_published: 2019-01-09T00:00:00Z
date_updated: 2023-09-19T10:10:55Z
day: '09'
ddc:
- '570'
department:
- _id: DaSi
doi: 10.1523/JNEUROSCI.1059-18.2018
ec_funded: 1
external_id:
isi:
- '000455189900006'
pmid:
- '30504274'
file:
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creator: dernst
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month: '01'
oa: 1
oa_version: Published Version
page: 238-255
pmid: 1
project:
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call_identifier: FP7
grant_number: '334077'
name: Investigating the role of transporters in invasive migration through junctions
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '8048'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila
and preserves the glial fate
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 39
year: '2019'
...
---
_id: '5'
abstract:
- lang: eng
text: In this paper, we introduce a quantum version of the wonderful compactification
of a group as a certain noncommutative projective scheme. Our approach stems from
the fact that the wonderful compactification encodes the asymptotics of matrix
coefficients, and from its realization as a GIT quotient of the Vinberg semigroup.
In order to define the wonderful compactification for a quantum group, we adopt
a generalized formalism of Proj categories in the spirit of Artin and Zhang. Key
to our construction is a quantum version of the Vinberg semigroup, which we define
as a q-deformation of a certain Rees algebra, compatible with a standard Poisson
structure. Furthermore, we discuss quantum analogues of the stratification of
the wonderful compactification by orbits for a certain group action, and provide
explicit computations in the case of SL2.
article_processing_charge: Yes (via OA deal)
author:
- first_name: Iordan V
full_name: Ganev, Iordan V
id: 447491B8-F248-11E8-B48F-1D18A9856A87
last_name: Ganev
citation:
ama: Ganev IV. The wonderful compactification for quantum groups. Journal of
the London Mathematical Society. 2019;99(3):778-806. doi:10.1112/jlms.12193
apa: Ganev, I. V. (2019). The wonderful compactification for quantum groups. Journal
of the London Mathematical Society. Wiley. https://doi.org/10.1112/jlms.12193
chicago: Ganev, Iordan V. “The Wonderful Compactification for Quantum Groups.” Journal
of the London Mathematical Society. Wiley, 2019. https://doi.org/10.1112/jlms.12193.
ieee: I. V. Ganev, “The wonderful compactification for quantum groups,” Journal
of the London Mathematical Society, vol. 99, no. 3. Wiley, pp. 778–806, 2019.
ista: Ganev IV. 2019. The wonderful compactification for quantum groups. Journal
of the London Mathematical Society. 99(3), 778–806.
mla: Ganev, Iordan V. “The Wonderful Compactification for Quantum Groups.” Journal
of the London Mathematical Society, vol. 99, no. 3, Wiley, 2019, pp. 778–806,
doi:10.1112/jlms.12193.
short: I.V. Ganev, Journal of the London Mathematical Society 99 (2019) 778–806.
date_created: 2018-12-11T11:44:06Z
date_published: 2019-06-01T00:00:00Z
date_updated: 2023-09-19T10:13:08Z
day: '01'
ddc:
- '510'
department:
- _id: TaHa
doi: 10.1112/jlms.12193
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- '000470025900008'
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file_size: 431754
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isi: 1
issue: '3'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '06'
oa: 1
oa_version: Published Version
page: 778-806
publication: Journal of the London Mathematical Society
publication_status: published
publisher: Wiley
publist_id: '8052'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The wonderful compactification for quantum groups
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 99
year: '2019'
...
---
_id: '7172'
abstract:
- lang: eng
text: "The development and growth of Arabidopsis thaliana is regulated by a combination
of genetic programing and also by the environmental influences. An important role
in these processes play the phytohormones and among them, auxin is crucial as
it controls many important functions. It is transported through the whole plant
body by creating local and temporal concentration maxima and minima, which have
an impact on the cell status, tissue and organ identity. Auxin has the property
to undergo a directional and finely regulated cell-to-cell transport, which is
enabled by the transport proteins, localized on the plasma membrane. An important
role in this process have the PIN auxin efflux proteins, which have an asymmetric/polar
subcellular localization and determine the directionality of the auxin transport.
During the last years, there were significant advances in understanding how the
trafficking molecular machineries function, including studies on molecular interactions,
function, subcellular localization and intracellular distribution. However, there
is still a lack of detailed characterization on the steps of endocytosis, exocytosis,
endocytic recycling and degradation. Due to this fact, I focused on the identification
of novel trafficking factors and better characterization of the intracellular
trafficking pathways. My PhD thesis consists of an introductory chapter, three
experimental chapters, a chapter containing general discussion, conclusions and
perspectives and also an appendix chapter with published collaborative papers.\r\nThe
first chapter is separated in two different parts: I start by a general introduction
to auxin biology and then I introduce the trafficking pathways in the model plant
Arabidopsis thaliana. Then, I explain also the phosphorylation-signals for polar
targeting and also the roles of the phytohormone strigolactone.\r\nThe second
chapter includes the characterization of bar1/sacsin mutant, which was identified
in a forward genetic screen for novel trafficking components in Arabidopsis thaliana,
where by the implementation of an EMS-treated pPIN1::PIN1-GFP marker line and
by using the established inhibitor of ARF-GEFs, Brefeldin A (BFA) as a tool to
study trafficking processes, we identified a novel factor, which is mediating
the adaptation of the plant cell to ARF-GEF inhibition. The mutation is in a previously
uncharacterized gene, encoding a very big protein that we, based on its homologies,
called SACSIN with domains suggesting roles as a molecular chaperon or as a component
of the ubiquitin-proteasome system. Our physiology and imaging studies revealed
that SACSIN is a crucial plant cell component of the adaptation to the ARF-GEF
inhibition.\r\nThe third chapter includes six subchapters, where I focus on the
role of the phytohormone strigolactone, which interferes with auxin feedback on
PIN internalization. Strigolactone moderates the polar auxin transport by increasing
the internalization of the PIN auxin efflux carriers, which reduces the canalization
related growth responses. In addition, I also studied the role of phosphorylation
in the strigolactone regulation of auxin feedback on PIN internalization. In this
chapter I also present my results on the MAX2-dependence of strigolactone-mediated
root growth inhibition and I also share my results on the auxin metabolomics profiling
after application of GR24.\r\nIn the fourth chapter I studied the effect of two
small molecules ES-9 and ES9-17, which were identified from a collection of small
molecules with the property to impair the clathrin-mediated endocytosis.\r\nIn
the fifth chapter, I discuss all my observations and experimental findings and
suggest alternative hypothesis to interpret my results.\r\nIn the appendix there
are three collaborative published projects. In the first, I participated in the
characterization of the role of ES9 as a small molecule, which is inhibitor of
clathrin- mediated endocytosis in different model organisms. In the second paper,
I contributed to the characterization of another small molecule ES9-17, which
is a non-protonophoric analog of ES9 and also impairs the clathrin-mediated endocytosis
not only in plant cells, but also in mammalian HeLa cells. Last but not least,
I also attach another paper, where I tried to establish the grafting method as
a technique in our lab to study canalization related processes."
acknowledged_ssus:
- _id: LifeSc
- _id: Bio
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Mina K
full_name: Vasileva, Mina K
id: 3407EB18-F248-11E8-B48F-1D18A9856A87
last_name: Vasileva
citation:
ama: Vasileva MK. Molecular mechanisms of endomembrane trafficking in Arabidopsis
thaliana. 2019. doi:10.15479/AT:ISTA:7172
apa: Vasileva, M. K. (2019). Molecular mechanisms of endomembrane trafficking
in Arabidopsis thaliana. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:7172
chicago: Vasileva, Mina K. “Molecular Mechanisms of Endomembrane Trafficking in
Arabidopsis Thaliana.” Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:7172.
ieee: M. K. Vasileva, “Molecular mechanisms of endomembrane trafficking in Arabidopsis
thaliana,” Institute of Science and Technology Austria, 2019.
ista: Vasileva MK. 2019. Molecular mechanisms of endomembrane trafficking in Arabidopsis
thaliana. Institute of Science and Technology Austria.
mla: Vasileva, Mina K. Molecular Mechanisms of Endomembrane Trafficking in Arabidopsis
Thaliana. Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:7172.
short: M.K. Vasileva, Molecular Mechanisms of Endomembrane Trafficking in Arabidopsis
Thaliana, Institute of Science and Technology Austria, 2019.
date_created: 2019-12-11T21:24:39Z
date_published: 2019-12-12T00:00:00Z
date_updated: 2023-09-19T10:39:33Z
day: '12'
ddc:
- '570'
degree_awarded: PhD
department:
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doi: 10.15479/AT:ISTA:7172
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month: '12'
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page: '192'
publication_identifier:
eissn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
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relation: part_of_dissertation
status: public
- id: '6377'
relation: part_of_dissertation
status: public
- id: '449'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Jiří
full_name: Friml, Jiří
id: 4159519E-F248-11E8-B48F-1D18A9856A87
last_name: Friml
orcid: 0000-0002-8302-7596
title: Molecular mechanisms of endomembrane trafficking in Arabidopsis thaliana
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...
---
_id: '6473'
abstract:
- lang: eng
text: "Single cells are constantly interacting with their environment and each other,
more importantly, the accurate perception of environmental cues is crucial for
growth, survival, and reproduction. This communication between cells and their
environment can be formalized in mathematical terms and be quantified as the information
flow between them, as prescribed by information theory. \r\nThe recent availability
of real–time dynamical patterns of signaling molecules in single cells has allowed
us to identify encoding about the identity of the environment in the time–series.
However, efficient estimation of the information transmitted by these signals
has been a data–analysis challenge due to the high dimensionality of the trajectories
and the limited number of samples. In the first part of this thesis, we develop
and evaluate decoding–based estimation methods to lower bound the mutual information
and derive model–based precise information estimates for biological reaction networks
governed by the chemical master equation. This is followed by applying the decoding-based
methods to study the intracellular representation of extracellular changes in
budding yeast, by observing the transient dynamics of nuclear translocation of
10 transcription factors in response to 3 stress conditions. Additionally, we
apply these estimators to previously published data on ERK and Ca2+ signaling
and yeast stress response. We argue that this single cell decoding-based measure
of information provides an unbiased, quantitative and interpretable measure for
the fidelity of biological signaling processes. \r\nFinally, in the last section,
we deal with gene regulation which is primarily controlled by transcription factors
(TFs) that bind to the DNA to activate gene expression. The possibility that non-cognate
TFs activate transcription diminishes the accuracy of regulation with potentially
disastrous effects for the cell. This ’crosstalk’ acts as a previously unexplored
source of noise in biochemical networks and puts a strong constraint on their
performance. To mitigate erroneous initiation we propose an out of equilibrium
scheme that implements kinetic proofreading. We show that such architectures are
favored over their equilibrium counterparts for complex organisms despite introducing
noise in gene expression. "
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Sarah A
full_name: Cepeda Humerez, Sarah A
id: 3DEE19A4-F248-11E8-B48F-1D18A9856A87
last_name: Cepeda Humerez
citation:
ama: Cepeda Humerez SA. Estimating information flow in single cells. 2019. doi:10.15479/AT:ISTA:6473
apa: Cepeda Humerez, S. A. (2019). Estimating information flow in single cells.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6473
chicago: Cepeda Humerez, Sarah A. “Estimating Information Flow in Single Cells.”
Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6473.
ieee: S. A. Cepeda Humerez, “Estimating information flow in single cells,” Institute
of Science and Technology Austria, 2019.
ista: Cepeda Humerez SA. 2019. Estimating information flow in single cells. Institute
of Science and Technology Austria.
mla: Cepeda Humerez, Sarah A. Estimating Information Flow in Single Cells.
Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6473.
short: S.A. Cepeda Humerez, Estimating Information Flow in Single Cells, Institute
of Science and Technology Austria, 2019.
date_created: 2019-05-21T00:11:23Z
date_published: 2019-05-23T00:00:00Z
date_updated: 2023-09-19T15:13:26Z
day: '23'
ddc:
- '004'
degree_awarded: PhD
department:
- _id: GaTk
doi: 10.15479/AT:ISTA:6473
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file_name: Thesis_Cepeda.zip
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date_created: 2019-05-23T11:18:13Z
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file_id: '6481'
file_name: CepedaThesis.pdf
file_size: 16646985
relation: main_file
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has_accepted_license: '1'
keyword:
- Information estimation
- Time-series
- data analysis
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: '135'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '1576'
relation: dissertation_contains
status: public
- id: '6900'
relation: dissertation_contains
status: public
- id: '281'
relation: dissertation_contains
status: public
- id: '2016'
relation: dissertation_contains
status: public
status: public
supervisor:
- first_name: Gašper
full_name: Tkačik, Gašper
id: 3D494DCA-F248-11E8-B48F-1D18A9856A87
last_name: Tkačik
orcid: 0000-0002-6699-1455
title: Estimating information flow in single cells
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: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2019'
...
---
_id: '6071'
abstract:
- lang: eng
text: 'Transcription factors, by binding to specific sequences on the DNA, control
the precise spatio-temporal expression of genes inside a cell. However, this specificity
is limited, leading to frequent incorrect binding of transcription factors that
might have deleterious consequences on the cell. By constructing a biophysical
model of TF-DNA binding in the context of gene regulation, I will first explore
how regulatory constraints can strongly shape the distribution of a population
in sequence space. Then, by directly linking this to a picture of multiple types
of transcription factors performing their functions simultaneously inside the
cell, I will explore the extent of regulatory crosstalk -- incorrect binding interactions
between transcription factors and binding sites that lead to erroneous regulatory
states -- and understand the constraints this places on the design of regulatory
systems. I will then develop a generic theoretical framework to investigate the
coevolution of multiple transcription factors and multiple binding sites, in the
context of a gene regulatory network that performs a certain function. As a particular
tractable version of this problem, I will consider the evolution of two transcription
factors when they transmit upstream signals to downstream target genes. Specifically,
I will describe the evolutionary steady states and the evolutionary pathways involved,
along with their timescales, of a system that initially undergoes a transcription
factor duplication event. To connect this important theoretical model to the prominent
biological event of transcription factor duplication giving rise to paralogous
families, I will then describe a bioinformatics analysis of C2H2 Zn-finger transcription
factors, a major family in humans, and focus on the patterns of evolution that
paralogs have undergone in their various protein domains in the recent past. '
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Roshan
full_name: Prizak, Roshan
id: 4456104E-F248-11E8-B48F-1D18A9856A87
last_name: Prizak
citation:
ama: Prizak R. Coevolution of transcription factors and their binding sites in sequence
space. 2019. doi:10.15479/at:ista:th6071
apa: Prizak, R. (2019). Coevolution of transcription factors and their binding
sites in sequence space. Institute of Science and Technology Austria. https://doi.org/10.15479/at:ista:th6071
chicago: Prizak, Roshan. “Coevolution of Transcription Factors and Their Binding
Sites in Sequence Space.” Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/at:ista:th6071.
ieee: R. Prizak, “Coevolution of transcription factors and their binding sites in
sequence space,” Institute of Science and Technology Austria, 2019.
ista: Prizak R. 2019. Coevolution of transcription factors and their binding sites
in sequence space. Institute of Science and Technology Austria.
mla: Prizak, Roshan. Coevolution of Transcription Factors and Their Binding Sites
in Sequence Space. Institute of Science and Technology Austria, 2019, doi:10.15479/at:ista:th6071.
short: R. Prizak, Coevolution of Transcription Factors and Their Binding Sites in
Sequence Space, Institute of Science and Technology Austria, 2019.
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title: Coevolution of transcription factors and their binding sites in sequence space
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