Lieven De Veylder Lab

Research focus

​How do plants cells know when to proliferate and when to stop dividing? To address these questions, Lieven De Veylder and his colleagues aim at identifying the mechanisms that link cell division with environmental stimuli.

Cell division is regulated by intriguing mechanisms, which ensure that the genome is replicated with high fidelity and distributed equally between the two daughter cells. In addition, the cell-cycle components are able to respond to signals from both the external environment and intrinsic developmental programs, resulting in the integration of cell division with the diverse developmental programs. Cyclin-dependent kinases (CDKs) play a central role in cell-cycle regulation. CDK activity is regulated by association with regulatory subunits: cyclins. The activity of the CDK/cyclin complexes is further controlled by a panoply of regulatory mechanisms including transcription, proteolysis, phosphorylation/dephosphorylation, interaction with regulatory proteins and intracellular trafficking.

The Cell Cycle Group aims to understand how CDKs and other related cell-cycle genes control cell division, and to elucidate how cell division control interacts with different aspects of plant development, such as morphogenesis, architecture and growth rate. In particular, the team aims to understand how plants control their exit from the cell cycle. In many plant species, this exit is accompanied by the onset of an alternative cycle known as the endocycle. Endoreplication represents a modified version of the normal mitotic cell cycle during which DNA is replicated without mitosis. The team focuses on molecular, biochemical and phenotypical analysis of transgenic plants in which the expression of key cell-cycle genes is modulated. As a model system, Arabidopsis thaliana is used, is which root and leaf cells gradually develop from a pure proliferating state into an endocycling mode. By growth analysis, combined with ploidy measurements, the effects of overexpression or knockdown of genes (or combination of genes) on the timing of endocycle onset is measured. By combining phenotypic analyses with transcript profiling experiments, we aim to identify the complete genetic and molecular network that regulates the endocycle, and thus cell cycle exit.

As a second major objective, the team aims to understand how plants adjust their cell cycle in response to the occurrence of DNA stress. Plants are sedentary, and so have unavoidably close contact with agents that target their genome integrity. To sense and react to these threats, plants have evolved DNA stress checkpoint mechanisms that arrest the cell cycle when DNA replication errors or DNA breaks occur. In this way, cells can repair the damaged DNA before entering mitosis, preventing the propagation of mutations. Although the pathways that maintain DNA integrity are largely conserved among eukaryotic organisms, plants put different accents on cell-cycle control under DNA stress. Through mutagenesis screens we aim to uncover the molecular components that account for these plant-specific responses.

Recently, the team adopted diatoms as a novel cell cycle model system. Among microalgae, diatoms represent not only one of the most species-rich classes, they are as well solely responsible for about 40% of all oceanic carbon fixation. Diatoms possess a highly chimeric genome arisen through endosymbiotic and horizontal bacterial gene transfers, resulting into a unique melting pot of diverse metabolic and biochemical pathways, likely contribution to their ability to their evolutionary and ecological success. As their proliferation depends strongly on stimuli such as light and nutrients, diatoms stand out as a model system to connect cell division with environmental conditions. Through the development of a molecular toolbox for diatoms, we aim at uncovering novel mechanism on how cells communicate with their environment.


Tissue-Specific Control of the Endocycle by the Anaphase Promoting Complex/Cyclosome Inhibitors UVI4 and DEL1Heyman Jefri Polyn Stefanie Eekhout Thomas De Veylder LievenPLANT PHYSIOLOGY, 175, 303-313, 2017
Deficiency of the Arabidopsis Helicase RTEL1 Triggers a SOG1-Dependent Replication Checkpoint in Response to DNA Cross-LinksHu Zhubing Cools Toon Kalhorzadeh Pooneh Heyman Jefri De Veylder LievenPLANT CELL, 27, 149-61, 2015
The Arabidopsis SIAMESE-RELATED cyclin-dependent kinase inhibitors SMR5 and SMR7 regulate the DNA damage checkpoint in response to reactive oxygen speciesYi D* Lessa Alvim Kamei C* Cools T Vanderauwera S Takahashi N Okushima Y Eekhout T Yoshiyama K Larkin J Van Den Daele H Conklin P Britt A Umeda M De Veylder LPLANT CELL, 26, 296-309, 2014* or °: authors contributed equally
Arabidopsis thaliana RNase H2 Deficiency Counteracts the Needs for the WEE1 Checkpoint Kinase but Triggers Genome InstabilityKalhorzadeh Pooneh Hu Zhubing Cools Toon Amiard S Willing E. M De Winne Nancy Gevaert Kris De Jaeger Geert Schneeberger K White C. L. 3rd De Veylder LievenPLANT CELL, 26, 3680-92, 2014
ERF115 controls root quiescent center cell division and stem cell replenishmentHeyman Jefri Cools Toon Vandenbussche F Heyndrickx Ken Van Leene Jelle Vercauteren Ilse Vanderauwera Sandy Vandepoele Klaas De Jaeger Geert Van Der Straeten D De Veylder LievenSCIENCE, 342, 860-3, 2013

Job openings


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24/10/2013 - Plant researchers at VIB and Ghent University discovered a new step in the complex regulation of stem cells. Today, their results are published online in this week’s issue of Science Express.

Lieven De Veylder

Lieven De Veylder

Research area(s)

Model organism(s)


​​Lieven De Veylder
PhD: Univ. of Ghent, Ghent, Belgium, 1998
VIB group leader since 2001

Contact Info

VIB-UGent Center for Plant Systems BiologyUGent-VIB Research Building FSVMTechnologiepark 71 9052 GENTRoute description