Caroline Sjogren / University of California, Riverside
Paul Larsen / University of California, Riverside,
Maren Heese / University Hamburg
Daniel Bouyer / Institut de Biologie de l’Ecole Normale Supérieure
Arp Schnittger / University of Hamburg
Aluminium (Al) ions are one of the primary growth-limiting factors for plants on acid soils, globally restricting agriculture. Despite its impact, little is known about Al action in planta. Earlier work has indicated that Al could induce DNA damage. However, it is not clear what kind of DNA damage is caused by Al and how it is repaired. These questions are especially important for plant breeding to find possibilities for growing of Al resistant plants. Here, we provide cytological and genetic evidence that exposure to Al leads to DNA double strand breaks. By applying a newly developed Al growth assay, we reveal that this damage specifically requires homologous recombination for repair. Testing different concentrations of Al, we find a multi-level response to Al-induced DNA damage that likely applies to other DNA damage response pathways. Analyzing the genome-wide binding pattern of the plant homolog of the animal tumor suppressor gene Retinoblastoma, we identify novel DDR genes that also function in response to Al. Among of them, KNOTEN 1 (KNO1) a novel DDR regulator, which is highly conserved in land plants. Loss of KNO1 leads to dramatic reduction in homologous recombination and conversely, KNO1 specially accumulates in meristem cells after exposure to DNA damaging drugs indicating that KNO1 is novel homologous recombination factor.