AtCAF‐1 mutants show different DNA damage responses after ultraviolet‐B than those activated by other genotoxic agents in leaves

Abstract

Chromatin assembly factor-1 (CAF-1) is a histone H3/H4 chaperone that participates in DNA and chromatin interaction processes. In this manuscript, we show that organs from CAF-1 deficient plants respond differently to ultraviolet-B (UV-B) radiation than to other genotoxic stresses. For example, CAF-1 deficient leaves tolerate better UV-B radiation, showing lower cyclobutane pyrimidine dimer (CPD) accumulation, lower inhibition of cell proliferation, increased cell wall thickness, UV-B absorbing compounds, and ploidy levels, whereas previous data from different groups have shown that CAF-1 mutants show shortening of telomeres, loss of 45S rDNA, and increased homologous recombination, phenotypes associated to DNA breaks. Interestingly, CAF-1 deficient roots show increased inhibition of primary root elongation, with decreased meristem size due to a higher inhibition of cell proliferation after UV-B exposure. The decrease in root meristem size in CAF-1 mutants is a consequence of defects in programmed cell death after UV-B exposure. Together, we provide evidence demonstrating that root and shoot meristematic cells may have distinct protection mechanisms against CPD accumulation by UV-B, which may be linked with different functions of the CAF-1 complex in these different organs.

Ultraviolet-B Radiation Represses Primary Root Elongation by Inhibiting Cell Proliferation in the Meristematic Zone of Arabidopsis Seedlings

“…Figure 4 shows that when UV-B irradiation was done when the meristematic zone is still growing (5 DAS), the number of dead cells was significantly higher than when the treatment was done after the meristem has reached its final size. Interestingly, 4 days after UV-B exposure, primary roots from irradiated seedlings at 5 DAS showed a significant reduction of dead cells, as previously reported ( Johnson et al, 2018 ; Maulión et al, 2019 ).…”

“…Together, these results demonstrate that exposure to UV-B at our experimental conditions affects cell proliferation in leaves and roots but only cell expansion in the root meristems. The increase in cell size could be a consequence of changes in the cell wall structure or composition occurring after exposure, as previously described in the leaf cell walls of mutants with altered sensitivity to this radiation ( Maulión et al, 2019 ), to changes in endoreduplication levels in the cells, which are sometimes measured after UV-B exposure in leaf cells ( Radziejwoski et al, 2011 ), or to other UV-B modulated mechanisms that could specifically affect cell size in the roots not yet characterized.…”

Arabidopsis mediator subunit 17 connects transcription with DNA repair after UV‐B exposure

“…When DNA damage occurs, DDRs are triggered, and one possible outcome of DDR is the PCD pathway, so as to avoid the propagation of mutations in case the damage is not properly repaired (Furukawa et al., 2010). In Arabidopsis, root and shoot stem cells specifically undergo PCD after they are exposed to different types of genotoxic stress conditions, such as radiomimetic drugs, X‐rays or UV‐B radiation (Fulcher & Sablowski, 2009; Furukawa et al., 2010; Maulión et al., 2019). DNA damage can be generated by different ambient conditions, such as chilling or by the oxidative stress produced by salinity or drought, for example (Hong et al., 2017).…”

“…Analysis was performed as described by Maulión et al. (2019). Briefly, total RNA was isolated using the TRIzol reagent (Invitrogen, now ThermoFisher Scientific); 0.5–1.0 mg of total RNA was reverse transcribed using SuperScript II reverse transcriptase (Invitrogen, now ThermoFisher Scientific) and oligo (dT) as a primer.…”

E2Fb and E2Fa transcription factors independently regulate the DNA damage response after ultraviolet B exposure in Arabidopsis

“…In particular, UV-B exposure significantly affects plant growth, inducing a reduction of the leaf area and inhibition of primary root elongation (Casadevall et al, 2013;Fierro et al, 2015;Fina et al, 2017;G omez et al, 2019;Wargent et al, 2009aWargent et al, , 2009b. In both leaves and roots, growth inhibition after UV-B exposure is because of a decrease in cell proliferation and/or in cell expansion; which may be affected differently by experimental conditions (G omez et al, 2019;Hectors et al, 2010;Mauli on et al, 2019). In particular, UV-B levels that produce DNA damage usually inhibit cell proliferation, whereas UV-B at lower doses and/or chronic irradiation can both inhibit cell proliferation and affect cell expansion (Dotto and Casati, 2017).…”