An Arabidopsis mutant atcsr-2 exhibits high cadmium stress sensitivity involved in the restriction of H2S emission.

The gene AtCSR encodes peptidyl-prolyl cis/trans isomerases (PPIases) that accelerate energetically unfavorable cis/trans isomerization of the peptide bond preceding proline production. In our studies, we found that AtCSR was associated with cadmium (Cd)-sensitive response in Arabidopsis. Our results show that AtCSR expression was triggered by Cd-stress in wild type Arabidopsis. The expression of some genes responsible for Cd(2+) transportation into vacuoles was induced, and the expression of the iron-regulated transporter 1 (IRT1) related to Cd(2+) absorption from the environment was not induced in wild type with Cd(2+) treatment. The expression of Cd-transportation related genes was not in response to Cd-stress, whereas IRT expression increased dramatically in atcsr-2 with Cd(2+) treatment. The expression of glutathione 1 (GSH1) was consistent with GSH being much lower in atcsr-2 in comparison with the wild type with Cd(2+) treatment. Additionally, malondialdehyde (MDA), hydrogen peroxide, and Cd(2+) contents, and activities of some antioxidative enzymes, differed between the wild type and atcsr-2. Hydrogen sulfide (H(2)S) has been confirmed as the third gas-transmitter over recent years. The findings revealed that the expression pattern of H(2)S-releasing related genes and that of Cd-induced chelation and transportation genes matched well in the wild type and atcsr-2, and H(2)S could regulate the expression of the Cd-induced genes and alleviate Cd-triggered toxicity. Finally, one possible suggestion was given: down-regulation of atcsr-2, depending on H(2)S gas-transmitter not only weakened Cd(2+) chelation, but also reduced Cd(2+) transportation into vacuoles, as well as enhancing the Cd(2+) assimilation, thus rendering atcsr-2 mutant sensitive to Cd-stress.