Maintaining food security in the context of climate change
Harnessing the DNA Damage Response to improve plant tolerance to heat stress
Microscopic visualization of DNA double-strand breaks in A. thaliana nuclei
The HeatDDR Doctoral Network
HeatDDR is a collaborative research initiative that brings together academic groups and private companies to uncover if and how the DNA Damage Response (DDR) contributes to heat stress–induced growth inhibition in plants. The HeatDDR consortium will train 9 international PhD students providing hands-on experience across diverse approaches in biochemistry, molecular biology, cell biology, genetics, computational biology, and plant phenotyping.
The project
Europe is facing food security challenges as a result of climate change. Increasingly frequent heat waves pose a major threat to crop yields, as heat stress inhibits plant growth. Research indicates that this growth reduction is likely to be linked to the activation of the plant DNA Damage Response (DDR), a mechanism that is also crucial for plant survival under the same conditions. Our project aims to decipher the connections between the DDR and stress-induced growth inhibition, with the ultimate goal of fine-tuning these cellular processes to supporting plant survival under stressful conditions without compromising growth.
The plant DNA Damage Response
The plant DNA Damage Response (DDR) is essential for survival under heat stress conditions. When exposed to heat, plants activate DDR to repair DNA lesions and maintain genome integrity, ensuring viability.
At the molecular level, DNA damage is sensed by the kinases ATR and ATM, which activate the transcription factor SOG1. SOG1, in turn, promotes the expression of genes responsible for cell cycle arrest (SMR5, SMR7, WEE1) and DNA repair (RAD51, BRCA2). The E2F/RBR module, together with the DREAM complex, further fine-tunes this transcriptional response. These mechanisms have been studied primarily in Arabidopsis, but they appear conserved in crops.
Recent evidence suggests that DDR activation may be responsible also for the growth inhibition observed in response to heat stress, likely by arresting the cell cycle, triggering cell death, and impairing stem cell function. Our project aims to test the hypothesis that stress-induced growth inhibition is a direct consequence of DDR activation.