Plant growth control during abiotic stress – GENOTOX

The scientific objective of this proposal is to identify the mechanisms by which plants arrest growth in response to abiotic stress. We will focus on genotoxic stress, which is caused by many environmental and physiological conditions plants are constantly exposed to, including ionizing radiation, high light intensities oxidative stress, and transposon excision. Double-strand breaks (DSBs) are mutagenic and potentially lethal.
A highly conserved surveillance and response system has evolved to cope with genotoxic stress. After perception of genotoxic stress, the protein kinases ATM and ATR are activated. ATM has many well-characterized targets in animal systems, but one of them stands out: the transcription factor p53. Activated p53 is the central transcriptional coordinator of downstream responses that include growth arrest, DNA repair, and apoptosis pathways. One of the key functions of p53 in animals is the arrest of cell cycle progression when activated, and this is accomplished by induction of p21, an inhibitor of cyclin-CDK activity. p53 also orchestrates DNA repair and programmed cell death. Thus, p53 acts as the ‘guardian of the genome’.
Many aspects of the genotoxic stress response and many regulatory components such as the ATM/ATR kinases are conserved, plants conspicuously lack a p53 ortholog, and up to now, no central ‘guardian of the genome’ has been identified. We have now identified two candidate genes that function to orchestrate genotoxic stress responses, the transcription factors TCP20 and SOG1. Evidence from our lab suggests that SOG1 and TCP20 interact to orchestrate the maintenance of plant genome integrity. We have also identified a key cell cycle regulator, the mitotic cyclin CycB1;1, as central regulator of growth arrest in response to genotoxic stress.
This project will focus on characterising their role in coordinating genotoxic stress responses and in arresting growth. We propose to examine how phosphorylation by ATM or ATR affects their activity and also to identify the CDK partner of cyclin CycB1;1 that is required for to mediate growth arrest. These tasks are of general importance, because TCP transcription factors are involved in coordinating cell growth and cell division in ‘normal’ conditions in plants. Thus, if TCP20 is required to control cell growth and proliferation both positively and negatively, it and other TCP genes are ultimately crucial for determining plant growth and yield.
The identification of regulators of abiotic stress is of general importance to secure continued high productivity of plants in the face of climate change. Most types of abiotic stress lead to transient growth arrest, which persists until the stress has passed, indicating that growth arrest is a protective measure to promote survival. To help identify the general mechanistic principles that underpin growth arrest during abiotic stress, we propose to also identify genes that mediate growth arrest during nutrient limitation. We have identified several mutants that define candidate growth regulators during phosphate starvation and propose to clone these.
Together, the identification of genes involved in controlling growth arrest in response to abiotic stress will allow us to fundamentally better understand how growth is controlled in plants and provide the tools to improve plant productivity in the long term by modifying growth control.