500 Gy) but greater than that resolvable by constitutively expressed DNA repair processes (e.g. We have typically used an acute, transiently growth-inhibiting 150-Gy dose, which is less than that triggering a permanent growth arrest (e.g.

In this work, we have used gamma irradiation for a ubiquitous induction of DNA damage throughout the seedling, with DSBs being the most cytotoxic lesion triggered ( Tounekti et al., 2001 Moiseenko et al., 2001). Here, we demonstrate the role of DDR genes in seedling recovery from growth-disruptive levels of DNA damage, which we have artificially induced by exposure to ionizing radiation (IR). In plants, DDR has a key role in the germination of seeds that have accumulated DNA damage during aging from desiccation/rehydration cycles, as repair is limited in the desiccated state ( Waterworth et al., 2015, 2016). These arrest and repair processes, together with programmed cell death ( Curtis and Hays, 2007) and the early induction of the endoreduplicative cell cycle ( Adachi et al., 2011), are collectively known as the DNA damage response (DDR), which safeguards the genomic integrity of the organism as a whole ( Yoshiyama, 2016).

DSBs are also potent inducers of checkpoint response, where cell cycle progression is transiently inhibited to allow for DNA repair before mitotic M phase ( Hu et al., 2016). Double-strand DNA breaks (DSBs) are particularly growth disruptive, leading to chromosome aberrations and mutations if incorrectly repaired and cell death if mitosis occurs before the repair of broken chromosomes ( Hu et al., 2016 Waterworth et al., 2015). DNA damage can cause cytostatic and cytotoxic effects, and can potentially lead to heritable mutations ( Waterworth et al., 2015).

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