Participation of Chromatin-Remodeling Proteins in the Repair of Ultraviolet-B-Damaged DNA      

Abstract

The genome of plants is organized into chromatin, affecting the rates of transcription, DNA recombination, and repair. In this work, we have investigated the consequences of reduced expression of some chromatin-remodeling factors and histone acetylation in maize (Zea mays) and Arabidopsis (Arabidopsis thaliana) in their participation in DNA repair after ultraviolet (UV)-B irradiation. Plants deficient in NFC102/NFC4 or SDG102/SDG26 showed more damaged DNA than wild-type plants; however, the Arabidopsis chc1 mutant showed similar accumulation of cyclobutane pyrimidine dimers as wild-type plants, in contrast to the increased DNA damage measured in the maize chc101 RNA interference line. In Arabidopsis, plants deficient in chromatin remodeling are also affected in the accumulation of pigments by UV-B. Plants treated with an inhibitor of histone acetyltransferases, curcumin, previous to the UV-B treatment show deficiencies in DNA repair; in addition, the chromatin remodeling-deficient plants have altered levels of acetylated histones after the UV-B treatment, demonstrating that histone acetylation is important during DNA repair in these two plant species. Arabidopsis mutants ham1 and ham2 also showed increased DNA damage after UV-B, suggesting that the role of these proteins in DNA damage repair has been conserved through evolution. However, cyclobutane pyrimidine dimer accumulation was higher in ham1 than in ham2; suggesting that HAM1 has a major role in DNA repair after UV-B. In summary, in this work, we have demonstrated that chromatin remodeling, and histone acetylation in particular, is important during DNA repair by UV-B, demonstrating that both genetic and epigenetic effects control DNA repair in plants.

ANTI-SILENCING FUNCTION1 Proteins Are Involved in Ultraviolet-Induced DNA Damage Repair and Are Cell Cycle Regulated by E2F Transcription Factors in Arabidopsis

“…Thus, chromatin structure regulates DNA damage signaling and histone modifications coordinate DNA repair (Sun et al, 2010). In accordance with these data, plant ham1 and ham2 mutants show increased DNA damage after UV-B irradiation (Campi et al, 2012). Therefore, the interaction between ASF1 and HAM proteins may be crucial to regulate cell cycle progression after a genotoxic stress.…”

“…In plants, E2F factors contribute to the transcriptional induction of genes upon DNA damage Shen, 2002;Ramirez-Parra and Gutierrez, 2007;Lincker et al, 2008). In addition, chromatin remodeling-deficient plants show increased DNA damage by UV-B (Campi et al, 2012). Thus, it is possible that AtASF1 proteins may have a role during DNA damage and repair.…”

SWP73 Subunits of Arabidopsis SWI/SNF Chromatin Remodeling Complexes Play Distinct Roles in Leaf and Flower Development

“…In addition, a homozygous SALK_113834 line carrying a T-DNA insertion in the SWP73B promoter region has been used in a study to demonstrate the involvement of SWP73B in DNA repair after UV-B treatment (Campi et al, 2012). Although this mutation was reported to reduce the SWP73B transcript level by 50% compared with the wild type (Campi et al, 2012), Jégu et al (2014) found that the line has wild-type SWP73B mRNA levels and is therefore not suitable for genetic analysis. Intriguingly, although this SALK_113834 mutant is distributed as a homozygous line, we found that it is in fact heterozygous and segregates the swp73b-1 T-DNA insertion allele.…”

“…Recently, these lines were found to show a late flowering phenotype under inductive long-day conditions (Jégu et al, 2014). In addition, a homozygous SALK_113834 line carrying a T-DNA insertion in the SWP73B promoter region has been used in a study to demonstrate the involvement of SWP73B in DNA repair after UV-B treatment (Campi et al, 2012). Although this mutation was reported to reduce the SWP73B transcript level by 50% compared with the wild type (Campi et al, 2012), Jégu et al (2014) found that the line has wild-type SWP73B mRNA levels and is therefore not suitable for genetic analysis.…”

“…Expression of SWP73B responds to UV-B treatment (Campi et al, 2012) and its RNA interference (RNAi) silencing results in dwarfism (Crane and Gelvin, 2007). SWP73B was identified as an interacting partner of cyclin-dependent kinase inhibitor KRP5 (KIP-RELATED PROTEIN5), suggesting a role in controlling the cell cycle and endoreduplication (Jégu et al, 2013).…”