Open AccessThe isothiocyanate sulforaphane induces respiratory burst oxidase homologue D‐dependent reactive oxygen species production and regulates expression of stress response genes
Author(s) -
Arruebarrena Di Palma Andrés,
Perk Enzo A.,
Carboni Martín E.,
GarcíaMata Carlos,
Budak Hikmet,
Tör Mahmut,
Laxalt Ana M.
Publication year - 2022
Publication title -
plant direct
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.211
H-Index - 11
ISSN - 2475-4455
DOI - 10.1002/pld3.437
Subject(s) - transcriptome , reactive oxygen species , sulforaphane , nadph oxidase , oxidative stress , microbiology and biotechnology , signal transduction , biology , arabidopsis , downregulation and upregulation , heat shock protein , gene expression , chemistry , gene , biochemistry , mutant
Abstract Sulforaphane (SFN) is an isothiocyanate‐type phytomolecule present in crucifers, which is mainly synthesized in response to biotic stress. In animals, SFN incorporated in the diet has anticancer properties among others. The mechanism of action and signaling are well described in animals; however, little is known in plants. The goal in the present study is to elucidate components of the SFN signaling pathway, particularly the production of reactive oxygen species (ROS), and its effect on the transcriptome. Our results showed that in Arabidopsis , SFN causes ROS production exclusively through the action of the NADPH oxidase RBOH isoform D that requires calcium as a signaling component for the ROS production. To add to this, we also analyzed the effect of SFN on the transcriptome by RNAseq. We observed the highest expression increase for heat shock proteins (HSP) genes and also for genes associated with the response to oxidative stress. The upregulation of several genes linked to the biotic stress response confirms the interplay between SFN and this stress. In addition, SFN increases the levels of transcripts related to the response to abiotic stress, as well as phytohormones. Taken together, these results indicate that SFN induces an oxidative burst leading to signaling events. This oxidative burst may cause the increase of the expression of genes such as heat shock proteins to restore cellular homeostasis and genes that codify possible components of the signaling pathway and putative effectors.