Abstract
Sulfur (S) assimilation, which is initiated by sulfate uptake, generates cysteine, the substrate for glutathione (GSH) and phytochelatin (PC) synthesis. GSH and PC contribute to cadmium (Cd) detoxification by capturing it for sequestration. Although Cd exposure is known to induce the expression of S-assimilating enzyme genes, including sulfate transporters (SULTRs), mechanisms of their transcriptional regulation are not well understood. Transcription factor SLIM1 controls transcriptional changes during S deficiency (−S) in Arabidopsis thaliana. We examined the potential involvement of SLIM1 in inducing the S assimilation pathway and PC accumulation. Cd treatment reduced the shoot fresh weight in the sulfur limitation1 (slim1) mutant but not in the parental line (1;2PGN). Cd-induced increases of sulfate uptake and SULTR1;2 expressions were diminished in the slim1 mutant, suggesting that SLIM1 is involved in inducing sulfate uptake during Cd exposure. The GSH and PC levels were lower in slim1 than in the parental line, indicating that SLIM1 was required for increasing PC during Cd treatment. Hence, SLIM1 indirectly contributes to Cd tolerance of plants by inducing −S responses in the cell caused by depleting the GSH pool, which is consumed by enhanced PC synthesis and sequestration to the vacuole.
Highlights
Cadmium (Cd) is highly toxic but non-essential for living organisms [1,2,3]
To define the contribution of the Sulfur LIMitation1 (SLIM1) transcription factor to plant tolerance for Cd, we compared the effects of Cd treatment on growth and Cd accumulation in a slim1 mutant, slim1–2, with those in the parental line, 1;2PGN (Figure 1a). 1;2PGN is a transgenic line harboring a fusion gene construct consisting of the 2,160 bp 50 -upstream region of SULTR1;2 and the coding region of GFP; this line accumulates GFP in response to −S [55]
The effects of Cd treatment and −S on the SULTR1;2 transcript level and the GFP fluorescence were similar in the 1;2PGN and slim1 mutants (Figure 5), which was consistent with the results presented in
Summary
Cadmium (Cd) is highly toxic but non-essential for living organisms [1,2,3]. It is released from natural and anthropogenic sources into the environment where it accumulates in the soil. GSH is a tri-peptide thiol synthesized from cysteine (Cys), glutamate (Glu), and glycine (Gly) by γ-glutamylcysteine synthetase (GSH1) and glutathione synthetase (GSH2). It contributes to Cd detoxification both as a scavenger of reactive oxygen species (ROS) and as a substrate of PC synthesis [13,19]. The importance of GSH and PC for Cd tolerance is indicated by the observation that certain mutations in either the PCS1 or GSH1 gene are associated with the Cd-sensitive phenotypes of the corresponding cad or cad mutants [25,26,27]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
