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An Arabidopsis mutant atcsr-2 exhibits high cadmium stress sensitivity involved in the restriction of HeS emission
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An Arabidopsis mutant atcsr-2 exhibits high cadmium stress sensitivity involved in the restriction of HeS emission
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An Arabidopsis mutant atcsr-2 exhibits high cadmium stress sensitivity involved in the restriction of HeS emission
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Journal Article
An Arabidopsis mutant atcsr-2 exhibits high cadmium stress sensitivity involved in the restriction of HeS emission
2012
Overview
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 Cd2＋ transportation into vacuoles was induced,and the expression of the iron-regulated transporter 1 （IRT1） related to Cd2＋ absorption from the environment was not induced in wild type with Cd2＋ treatment.The expression of Cd-transportation related genes was not in response to Cd-stress,whereas IRT expression increased dramatically in atcsr-2 with Cd2＋ treatment.The expression of glutathione 1 （GSH1） was consistent with GSH being much lower in atcsr-2 in comparison with the wild type with Cd2＋ treatment.Additionally,malondialdehyde （MDA）,hydrogen peroxide,and Cd2＋ contents,and activities of some antioxidative enzymes,differed between the wild type and atcsr-2.Hydrogen sulfide （H2S） has been confirmed as the third gas-transmitter over recent years.The findings revealed that the expression pattern of H2 S-releasing related genes and that of Cd-induced chelation and transportation genes matched well in the wild type and atcsr-2,and H2S 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 H2S gas-transmitter not only weakened Cd2＋ chelation,but also reduced Cd2＋ transportation into vacuoles,as well as enhancing the Cd2＋ assimilation,thus rendering atcsr-2 mutant sensitive to Cd-stress.
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