A role for UV-B -induced DNA damage in photomorphogenic responses in etiolated Arabidopsis seedlings

Ultraviolet (UV) radiation is a constituent of sunlight that influences plant morphology and growth. It induces photomorphogenic responses but also causes damage to DNA. Plant responses to DNA damage caused by UV-B light are often categorized as general mechanisms that get activated by other environmental stresses. Photodimers are formed through the direct absorption of UV-B light by DNA and are removed, in part, by nucleotide excision repair (NER). UV-B irradiation resulted in the accumulation of the two most common photodimers, cyclobutane pyrimidine dimers (CPDs) and pyrimidine-(6,4)-pyrimidinone dimers (6,4PPs), in etiolated wild type (wt) Arabidopsis seedlings. Arabidopsis mutants of the endonucleases that function in NER, xpf-3 and uvr1-1, show hypersensitivity to UV-B (280-320 nm) in terms of hypocotyl growth inhibition. I hypothesized that the accumulation of UV-B-induced photodimers was responsible for the hypocotyl growth phenotype of these NER mutants after UV-B irradiation. It was also predicted that the accumulation of photodimers could ultimately trigger signaling pathways that result in cell-cycle arrest through stalled replication sites or double-strand breaks. This was tested using the suppressor of gamma 1 (sog1-1) mutant, which lacks a transcription factor responsible for gene induction and cell-cycle arrest after gamma irradiation, and a Col-0 line containing a CYCB1;1-GUS reporter construct. CYCB1;1 encodes a cyclin that accumulates in response to cell-cycle arrest at the G2/M transition. The main conclusion from this work is that hypocotyl growth inhibition induced by UV-B light in etiolated Arabidopsis seedlings, which is a classic photomorphogenic response, is influenced by signals originating from UV-B light absorption by DNA that lead to cell-cycle arrest. Furthermore, this process is shown to occur independently of UVR8 and its signaling pathway responsible for CHS induction. This work also demonstrates that UV-B-induced DNA damage can be responsible for specific photomorphogenic responses, at least in etiolated Arabidopsis seedlings, and does not simply induce general stress responses.