PDCD5 protein plays a role in programmed cell death after UV-B exposure in Arabidopsis

FALCONE FERREYRA, M.L.; CASADEVALL, ROMINA; D'ANDREA, L.; CASATI, P.

Foz de Iguazu

Congreso; 11th International congress of plant molecular biology; 2015

DNA damage responses have evolved to sense and react to DNA damage; the induction of DNA repair mechanisms can lead to genomic restoration or, if the damaged DNA cannot be adequately repaired, to the execution of a cell death program. Chromatin remodeling, and histone acetylation in particular, are important epigenetic mechanisms involved in DNA damage repair induced by UV-B radiation in plants. In human, PDCD5 protein is an important regulator of TIP60, the homolog of Arabidopsis HAM1 and HAM2 Histone acetyltransferases. In this work, we investigate the role of an Arabidopsis protein, AtPDCD5, which is highly similar to the human PDCD5 protein and participates in programmed cell death (PCD) in the UV-B DNA damage response. AtPDCD5 expression is induced by UV-B radiation and transgenic plants expressing AtPDCD5 fused to GFP indicate that AtPDCD5 is localized both in the nucleus and the cytosol. pdcd5 mutant plants exhibited an altered antioxidant metabolism and accumulated higher levels of DNA damage after UV-B exposure, similar to levels in ham1ham2 RNAi transgenic lines with decreased expression of acetyltransferases from the MYST family. Coimmunoprecipitation and pull down assays showed that AtPDCD5 interacts with HAM proteins, suggesting that both proteins participate in the same pathway of DNA damage repair. Finally, plants overexpressing AtPDCD5 showed less DNA damage but more cell death in root tips upon UV-B exposure. Together, the results described demonstrate that AtPDCD5 plays an important role during DNA damage responses induced by UV-B radiation in Arabidopsis.