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Auxin-dependent cell cycle reactivation through transcriptional regulation of Arabidopsis E2Fa by lateral organ boundary proteins

Barbara Berckmans UGent, Valya Vassileva UGent, Stephan PC Schmid, Sara Maes UGent, Boris Parizot UGent, Satoshi Naramoto UGent, Zoltan Magyar, Claire Lessa Alvim Kamei UGent, Csaba Koncz and Laszlo Bogre, et al. (2011) PLANT CELL. 23(10). p.3671-3683
abstract
Multicellular organisms depend on cell production, cell fate specification, and correct patterning to shape their adult body. In plants, auxin plays a prominent role in the timely coordination of these different cellular processes. A well-studied example is lateral root initiation, in which auxin triggers founder cell specification and cell cycle activation of xylem pole-positioned pericycle cells. Here, we report that the E2Fa transcription factor of Arabidopsis thaliana is an essential component that regulates the asymmetric cell division marking lateral root initiation. Moreover, we demonstrate that E2Fa expression is regulated by the LATERAL ORGAN BOUNDARY DOMAIN18/LATERAL ORGAN BOUNDARY DOMAIN33 (LBD18/LBD33) dimer that is, in turn, regulated by the auxin signaling pathway. LBD18/LBD33 mediates lateral root organogenesis through E2Fa transcriptional activation, whereas E2Fa expression under control of the LBD18 promoter eliminates the need for LBD18. Besides lateral root initiation, vascular patterning is disrupted in E2Fa knockout plants, similarly as it is affected in auxin signaling and lbd mutants, indicating that the transcriptional induction of E2Fa through LBDs represents a general mechanism for auxin-dependent cell cycle activation. Our data illustrate how a conserved mechanism driving cell cycle entry has been adapted evolutionarily to connect auxin signaling with control of processes determining plant architecture.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
ARF19, DOMAIN, LEAVES, DIFFERENTIATION, THALIANA, AS2/LOB FAMILY, GENE-EXPRESSION, PLANT DEVELOPMENT, TANDEM AFFINITY PURIFICATION, ROOT INITIATION
journal title
PLANT CELL
Plant Cell
volume
23
issue
10
pages
3671 - 3683
Web of Science type
Article
Web of Science id
000298175900011
JCR category
PLANT SCIENCES
JCR impact factor
8.987 (2011)
JCR rank
5/189 (2011)
JCR quartile
1 (2011)
ISSN
1040-4651
DOI
10.1105/tpc.111.088377
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1996014
handle
http://hdl.handle.net/1854/LU-1996014
date created
2012-01-19 10:52:06
date last changed
2012-12-17 16:45:00
@article{1996014,
  abstract     = {Multicellular organisms depend on cell production, cell fate specification, and correct patterning to shape their adult body. In plants, auxin plays a prominent role in the timely coordination of these different cellular processes. A well-studied example is lateral root initiation, in which auxin triggers founder cell specification and cell cycle activation of xylem pole-positioned pericycle cells. Here, we report that the E2Fa transcription factor of Arabidopsis thaliana is an essential component that regulates the asymmetric cell division marking lateral root initiation. Moreover, we demonstrate that E2Fa expression is regulated by the LATERAL ORGAN BOUNDARY DOMAIN18/LATERAL ORGAN BOUNDARY DOMAIN33 (LBD18/LBD33) dimer that is, in turn, regulated by the auxin signaling pathway. LBD18/LBD33 mediates lateral root organogenesis through E2Fa transcriptional activation, whereas E2Fa expression under control of the LBD18 promoter eliminates the need for LBD18. Besides lateral root initiation, vascular patterning is disrupted in E2Fa knockout plants, similarly as it is affected in auxin signaling and lbd mutants, indicating that the transcriptional induction of E2Fa through LBDs represents a general mechanism for auxin-dependent cell cycle activation. Our data illustrate how a conserved mechanism driving cell cycle entry has been adapted evolutionarily to connect auxin signaling with control of processes determining plant architecture.},
  author       = {Berckmans, Barbara and Vassileva, Valya and Schmid, Stephan PC and Maes, Sara and Parizot, Boris and Naramoto, Satoshi and Magyar, Zoltan and Lessa Alvim Kamei, Claire and Koncz, Csaba and Bogre, Laszlo and Persiau, Geert and De Jaeger, Geert and Friml, Jiri and Simon, R and Beeckman, Tom and De Veylder, Lieven},
  issn         = {1040-4651},
  journal      = {PLANT CELL},
  keyword      = {ARF19,DOMAIN,LEAVES,DIFFERENTIATION,THALIANA,AS2/LOB FAMILY,GENE-EXPRESSION,PLANT DEVELOPMENT,TANDEM AFFINITY PURIFICATION,ROOT INITIATION},
  language     = {eng},
  number       = {10},
  pages        = {3671--3683},
  title        = {Auxin-dependent cell cycle reactivation through transcriptional regulation of Arabidopsis E2Fa by lateral organ boundary proteins},
  url          = {http://dx.doi.org/10.1105/tpc.111.088377},
  volume       = {23},
  year         = {2011},
}

Chicago
Berckmans, Barbara, Valya Vassileva, Stephan PC Schmid, Sara Maes, Boris Parizot, Satoshi Naramoto, Zoltan Magyar, et al. 2011. “Auxin-dependent Cell Cycle Reactivation Through Transcriptional Regulation of Arabidopsis E2Fa by Lateral Organ Boundary Proteins.” Plant Cell 23 (10): 3671–3683.
APA
Berckmans, B., Vassileva, V., Schmid, S. P., Maes, S., Parizot, B., Naramoto, S., Magyar, Z., et al. (2011). Auxin-dependent cell cycle reactivation through transcriptional regulation of Arabidopsis E2Fa by lateral organ boundary proteins. PLANT CELL, 23(10), 3671–3683.
Vancouver
1.
Berckmans B, Vassileva V, Schmid SP, Maes S, Parizot B, Naramoto S, et al. Auxin-dependent cell cycle reactivation through transcriptional regulation of Arabidopsis E2Fa by lateral organ boundary proteins. PLANT CELL. 2011;23(10):3671–83.
MLA
Berckmans, Barbara, Valya Vassileva, Stephan PC Schmid, et al. “Auxin-dependent Cell Cycle Reactivation Through Transcriptional Regulation of Arabidopsis E2Fa by Lateral Organ Boundary Proteins.” PLANT CELL 23.10 (2011): 3671–3683. Print.