Transcriptomics and Functional Genomics of ROS-Induced Cell Death Regulation by RADICAL-INDUCED CELL DEATH1

Abstract

Plant responses to changes in environmental conditions are mediated by a network of signaling events leading to downstream responses, including changes in gene expression and activation of cell death programs. Arabidopsis thaliana RADICAL-INDUCED CELL DEATH1 (RCD1) has been proposed to regulate plant stress responses by protein-protein interactions with transcription factors. Furthermore, the rcd1 mutant has defective control of cell death in response to apoplastic reactive oxygen species (ROS). Combining transcriptomic and functional genomics approaches we first used microarray analysis in a time series to study changes in gene expression after apoplastic ROS treatment in rcd1. To identify a core set of cell death regulated genes, RCD1-regulated genes were clustered together with other array experiments from plants undergoing cell death or treated with various pathogens, plant hormones or other chemicals. Subsequently, selected rcd1 double mutants were constructed to further define the genetic requirements for the execution of apoplastic ROS induced cell death. Through the genetic analysis we identified WRKY70 and SGT1b as cell death regulators functioning downstream of RCD1 and show that quantitative rather than qualitative differences in gene expression related to cell death appeared to better explain the outcome. Allocation of plant energy to defenses diverts resources from growth. Recently, a plant response termed stress-induced morphogenic response (SIMR) was proposed to regulate the balance between defense and growth. Using a rcd1 double mutant collection we show that SIMR is mostly independent of the classical plant defense signaling pathways and that the redox balance is involved in development of SIMR.

Circadian Stress Regimes Affect the Circadian Clock and Cause Jasmonic Acid-Dependent Cell Death in Cytokinin-Deficient Arabidopsis Plants

“…The expression levels of JAZ1 (and BI1) correlated well with the severity of cell death in cytokinin-deficient plants (Figure 12; Supplemental Figure 4). This is consistent with results showing that quantitative differences in cell death-related gene expression better correlated with the observed cell death phenotypes than qualitative changes (Brosché et al, 2014). This finding also indicates that the extent to which the JA pathway is activated is a decisive factor in determining the severity of circadian stress-induced PCD.…”

Sequencing of allotetraploid cotton (Gossypium hirsutum L. acc. TM-1) provides a resource for fiber improvement

“…In the D subgenome, 54 upregulated PSGs (Supplementary Table 20) are related to salt and/or osmotic stress tolerance, response to superoxide and ethylene, and include radical-induced cell death 1 gene (RCD1) 44 (Gh_D08G1685) and aldehyde dehydrogenase 7 (ALDH7) 45 (Gh_D06G1578) (Supplementary Fig. 17).…”

Roles of Defense Hormones in the Regulation of Ozone-Induced Changes in Gene Expression and Cell Death

“…Apart from cell death, apoplastic ROS signaling also triggers broad transcriptional responses, where the expression of thousands of genes is altered (Blomster et al, 2011;Brosché et al, 2014). Very few transcription factors (TFs) mediating this response have been identified to date.…”