Abstract
All processes requiring interaction with DNA are attuned to occur within the context of the complex chromatin structure. As it does for programmed transcription and replication, this also holds true for unscheduled events, such as repair of DNA damage. Lesions such as double-strand breaks occur randomly; their repair requires that enzyme complexes access DNA at potentially any genomic site. This is achieved by chromatin remodeling factors that can locally slide, evict, or change nucleosomes. Here, we show that the Swi2/Snf2-related (SWR1 complex), known to deposit histone H2A.Z, is also important for DNA repair in Arabidopsis thaliana. Mutations in genes for Arabidopsis SWR1 complex subunits photoperiod-independent Early Flowering1, actin-related protein6, and SWR1 complex6 cause hypersensitivity to various DNA damaging agents. Even without additional genotoxic stress, these mutants show symptoms of DNA damage accumulation. The reduced DNA repair capacity is connected with impaired somatic homologous recombination, in contrast with the hyper-recombinogenic phenotype of yeast SWR1 mutants. This suggests functional diversification between lower and higher eukaryotes. Finally, reduced fertility and irregular gametogenesis in the Arabidopsis SWR1 mutants indicate an additional role for the chromatin-remodeling complex during meiosis. These results provide evidence for the importance of Arabidopsis SWR1 in somatic DNA repair and during meiosis.
Highlights
Double-strand breaks (DSBs) are a deleterious type of DNA damage, and their quick and efficient removal is of the utmost importance, as a single unrepaired DSB can be lethal to cells (Bennett et al, 1993)
We show that pie1-3, arp6-3, and swc6-1 are hypersensitive to DNA damage-inducing agents and display signs of accumulated DNA damage
We tested the response to UV-C exposure and observed reduced resistance in pie1, arp6, and swc6, which was evident by high numbers of seedlings with reduced size, chlorotic cotyledons, and death 8 d after treatment (Figure 1F)
Summary
Double-strand breaks (DSBs) are a deleterious type of DNA damage, and their quick and efficient removal is of the utmost importance, as a single unrepaired DSB can be lethal to cells (Bennett et al, 1993). DSB repair is accomplished by two main pathways: nonhomologous end joining (NHEJ) and homologous recombination (HR). HR is a more complex and more conservative mechanism in which intact homologous regions are used as a template for repair (reviewed in Heyer et al, 2010). The molecular mechanisms that control DSB signaling and repair by both pathways have been characterized and reviewed extensively (Schuermann et al, 2005; Heyer et al, 2010; Knoll and Puchta, 2011; Waterworth et al, 2011). Surprisingly little is known about how DSB repair is regulated in the context of chromatin, an important aspect since DNA lesions occur within the context of the complex higher order structure of chromatin
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