Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/38916
Title: PHYTOCHELATIN PRODUCTION IS ESSENTIAL TO INDUCE THE DNA DAMAGE RESPONSE AND MAINTAIN VEGETATIVE GROWTH IN CADMIUM-EXPOSED ARABIDOPSIS THALIANA
Authors: IVEN, Verena 
HENDRIX, Sophie 
CUYPERS, Ann 
Issue Date: 2021
Source: INTERNATIONAL CONFERENCE ON PLANT SYSTEMS BIOLOGY AND BIOTECHNOLOGY (ICPSBB), Bulgaria, 14-17/06/2021
Abstract: Environmental cadmium (Cd) contamination is a worldwide problem as Cd can readily be taken up by plants, hereby disturbing their growth and development. Important molecules in the defence against Cd phytotoxicity are the Cd-chelating phytochelatins (PCs), which are oligomers derived from glutathione. Previous analyses in the glutathione-deficient cadmium-sensitive 2-1 (cad2-1) mutant demonstrated that glutathione is involved in the DNA damage response (DDR), regulating cell cycle progression, DNA repair and programmed cell death, in both roots and leaves of Cd-exposed A. thaliana (1). The main goal of this study was to determine whether these effects on the DDR are caused by a reduced PC content rather than the absence of glutathione as an antioxidant. In order to do so, wild-type (WT) and PC-deficient cad1-3 plants were exposed to 0, 2 and 5 µM CdSO4 and effects on endoreplication, vegetative growth and transcription of cell cycle and DNA repair genes were assessed. Results displayed more pronounced inhibition of growth and endoreplication in cad1-3 plants upon Cd exposure. This coincided with a downregulated expression of cell cycle genes in this mutant compared to WT plants. In addition, the DDR appeared to be altered in cad1-3 plants as DNA damage and repair genes were induced by Cd exposure in WT, but not in mutant plants. The obtained results, combined with the previous findings of Hendrix et al. suggest that phytochelatin production is essential to induce the DDR in Cd-exposed A. thaliana.
Document URI: http://hdl.handle.net/1942/38916
Category: C2
Type: Conference Material
Appears in Collections:Research publications

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