[Seminars] PSB event reminder
contact at psb.vib-ugent.be
contact at psb.vib-ugent.be
Fri Oct 12 12:10:01 CEST 2012
Calendar Name: seminars
Scheduled for: Friday, October 12 2012, 14:00 - 15:30
Event text: Dr Arp Schnittger
Department of Molecular Mechanisms of Phenotypic
Plasticity
Institut de Biologie Moléculaire des Plantes du CNRS
Université de Strasbourg
Strasbourg
FRANCE
Details: How to make stable decisions in cell proliferation and
differentiation
ABSTRACT
The decision to replicate its DNA is of crucial
importance for every cell and in many organisms decisive
to progress through the entire cell cycle. Using pollen
as a model system, we have identified a general
regulatory cascade controlling entry into S phase in
many if not all Arabidopsis cells. This cascade
comprises the Arabidopsis homologs of the animal
transcription factor E2F, the plant homolog of the
animal transcriptional repressor Retinoblastoma
(Rb)-related 1 (RBR1), the plant-specific F-box protein,
F-BOX-LIKE 17, the plant specific cyclin-dependent
kinase (CDK) inhibitors KRPs, as well as CDKA;1, the
plant homolog of the yeast and animal Cdc2+/Cdk1
kinases. Biomathematical simulations and subsequent
experimental confirmation of computational predictions
revealed that this regulatory circuit can give rise to
hysteresis highlighting the identified dosage
sensitivity of CDK inhibitors in this network.
Remarkably, many components of this cell cycle control
module appear to function in the control of asymmetric
division and cell fate specification as well. I will
present data from our team showing that RBR1 not only
controls cell proliferation but also cell
differentiation genes during root meristem and stomata
development. This leads to a CDKA;1-dose dependent model
of formative divisions in which low and medium levels of
CDKA;1 are sufficient for symmetric divisions but high
kinase levels being required for asymmetric divisions.
An important aspect of this wiring is again the
hysteretic behavior of the system revealing an intimate
connection between cell cycle progression and cell fate
acquisition.
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