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Aluminium (Al) toxicity is an important limitation to worldwide crop production, occurring in upwards of 50 % of the world’s arable land. The most evident symptom and important consequence of Al toxicity is root growth inhibition on acidic soils. A prominent example is barley, which is one of the most important crops in temperate regions including Europe and North America. Barley is very sensitive to Al toxicity and yield losses of up to 30 % have been associated with growth at low pH. It has been previously argued that Al toxicity was an intractable problem due to its apparent complexity. However, our preparatory work in the model plant Arabidopsis thaliana has recently shown that this growth inhibition results at least in part from activation of an ATM AND RAD3-RELATED (ATR)- dependent cell cycle arrest program in response to Al-dependent damage. The finding that Al act as a DNA-stress inducing compound represents a new perspective on Al toxicity that bears further investigation. Here, we will use Arabidopsis and barley as model systems to study this novel effect of Al. To this end, we will first discern through Next Generation Sequencing the nature of DNA damage exerted by Al, especially because Al has not been found to have similar consequences as other DNA damaging agents affecting biomass, such as UV-B and high light. Next, through the combination of transcriptomics, phylogenetics, and phenotypic analyses, we aim to uncover the conserved molecular framework underlying an Al-induced cell cycle arrest. As a complement, available cell cycle checkpoint mutants will be tested for their response to Al treatment and used to identify novel signaling components through (phospho)proteomics and a suppressor mutagenesis screen. Finally, through the combination of translation of results from Arabidopsis to barely and primary result-driven research in barely, we will exploit checkpoint control research to confer Al tolerance in crop species. |