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

Ultraviolet (UV)B radiation affects plant growth inhibiting cell proliferation. This inhibition is in part controlled by the activity of transcription factors from the E2F family. In particular, the participation of E2Fc and E2Fe in UV-B responses in Arabidopsis plants was previously reported. However, the E2Fa and E2Fb contribution to these processes has still not been investigated. Thus, in this work, we provide evidence that, in Arabidopsis, both E2Fa and E2Fb control leaf size under UV-B conditions without participating in the repair of cyclobutane pyrimidine dimers in the DNA. Nevertheless, in UV-B-exposed seedlings, E2Fa, but not E2Fb, regulates primary root elongation, cell proliferation, and programmed cell death in the meristematic zone. Using e2fa mutants that overexpress E2Fb, we showed that the role of E2Fa in the roots could not be replaced by E2Fb. Finally, our results show that E2Fa and E2Fb differentially regulate the expression of genes that activate the DNA damage response and cell cycle progression, both under conditions without UV-B and after exposure. Overall, we showed that both E2Fa and E2Fb have different and non-redundant roles in developmental and DNA damage responses in Arabidopsis plants exposed to UV-B.

Chromatin dynamics during DNA damage and repair in plants: new roles for old players.

The genome of plants is organized into chromatin. The chromatin structure regulates the rates of DNA metabolic processes such as replication, transcription, DNA recombination, and repair. Different aspects of plant growth and development are regulated by changes in chromatin status by the action of chromatin-remodeling activities. Recent data have also shown that many of these chromatin-associated proteins participate in different aspects of the DNA damage response, regulating DNA damage and repair, cell cycle progression, programmed cell death, and entry into the endocycle. In this review, we present different examples of proteins and chromatin-modifying enzymes with roles during DNA damage responses, demonstrating that rapid changes in chromatin structure are essential to maintain genome stability.

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

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.

UV-B radiation delays flowering time through changes in the PRC2 complex activity and miR156 levels in Arabidopsis thaliana.

UV-B is a high-energy component of the solar radiation perceived by the plant and induces a number of modifications in plant growth and development, including changes in flowering time. However, the molecular mechanisms underlying these changes are largely unknown. In the present work, we demonstrate that Arabidopsis plants grown under white light supplemented with UV-B show a delay in flowering time, and this developmental reprogramming is mediated by the UVR8 photoreceptor. Using a combination of gene expression analyses and UV-B irradiation of different flowering mutants, we gained insight into the pathways involved in the observed flowering time delay in UV-B-exposed Arabidopsis plants. We provide evidence that UV-B light downregulates the expression of MSI1 and CLF, two of the components of the polycomb repressive complex 2, which in consequence drives a decrease in H3K27me3 histone methylation of MIR156 and FLC genes. Modification in the expression of several flowering time genes as a consequence of the decrease in the polycomb repressive complex 2 activity was also determined. UV-B exposure of flowering mutants supports the involvement of this complex in the observed delay in flowering time, mostly through the age pathway.