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

• Published in: Plant, cell and environment Vol. 42; no. 9; pp. 2730 - 2745
• Main Authors: Maulión, Evangelina, Gomez, María Sol, Bustamante, Claudia Anabel, Casati, Paula
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01-09-2019
• Subjects: Accumulation; Apoptosis; Arabidopsis - genetics; Arabidopsis - metabolism; Arabidopsis - radiation effects; Arabidopsis Proteins - genetics; Cell death; Cell growth; Cell Proliferation; Cell Wall - metabolism; Cell walls; chromatin; Chromatin remodeling; Compounds; Cyclobutane; Deoxyribonucleic acid; Dimers; DNA; DNA Damage; Elongation; Endoreduplication; Genotoxic chemicals; Genotoxicity; histone chaperones; Histone H3; Homologous recombination; Homology; Leaves; Lymphocytes B; Meristems; Organs; Phenotypes; Pigments, Biological - metabolism; Plant Leaves - metabolism; Plant Leaves - radiation effects; Plant Roots - metabolism; Plant Roots - radiation effects; Ploidy; RNA Splicing Factors - genetics; Telomeres; Ultraviolet radiation; Ultraviolet Rays; UV‐B radiation; Wall thickness; histone chaperones; cell proliferation; UV-B radiation; chromatin; DNA damage
• ISSN: 0140-7791; 1365-3040
• DOI: 10.1111/pce.13596

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.
We provide evidence that demonstrate that ultraviolet‐B (UV‐B) radiation that produce cyclobutane pyrimidine dimers activate different DNA damage response mechanisms than other DNA‐damaging agents, which require chromatin assembly factor‐1 activity, and that root and shoot meristematic cells may have distinct protection mechanisms against DNA damage by UV‐B.