Research focus
How do plants cells know when to stop dividing? To address this question, Lieven De Veylder and his colleagues study an alternative cell cycle that marks the onset of cell differentiation. Identifying the mechanisms that control the timing of cell cycle exit might open opportunities to adjust plant size and architecture.
Cell division is regulated by intriguing mechanisms which ensure that DNA 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, we aim 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. Endoreduplication 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, the first leaf pair of Arabidopsis thaliana is used, which gradually develops from a pure proliferating state into an endocycling mode. By kinematic 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 errs 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.