Functional-structural analysis of Casein Kinase 2 and SOG1 in response to Al-induced DNA damage and phosphate starvation

Aluminum (Al) toxicity represents 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. Additionally, Al influences
phosphorus (Pi) availability, eventually resulting in nutritional deficiency in shoots and leaves. Recently, we have identified through a chemical genomics screen in Arabidopsis thaliana a compound (nominated C43) that confers Al resistance, being a potential Casein Kinase 2 (CK2) inhibitor. Our preliminary data indicate that CK2 grants Al toxicity resistance through phosphorylation of the SOG1 transcription factor, being an essential regulator arresting cell cycle progression in response to DNA damage. Strikingly, C43 also grants growth under low Pi conditions, suggesting that Pi-deficiency and Al- toxicity converge via the CK2-SOG1 pathway. Within this project, we aim to test this hypothesis through a detailed structural-functional analysis in combination with physiological experiments. In particular, the interactions between C43, CK2 and SOG1 will be studies at the biochemical, biophysical and structural level. Additionally, the obtained structural data will be correlated with growth experiments under conditions of Al toxicity and Pi depletion.