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Formaldehyde (HCHO) is a major indoor air pollutant. Plants can be used to remove HCHO from polluted air because they can use HCHO as a carbon source to incorporate it into one-carbon (C1) metabolism. However, high concentrations of exogenous HCHO cause damages to plants. Therefore, genetic engineering is an effective measure to improve ability of plants to clear the HCHO pollution. Expression of AtHsfA1d encoding heat shock transcription factor of Arabidopsis was induced by HCHO stress. AtHsfA1d was cloned into the pYES3 vector and transformed into Saccharomyces cerevisiae. Yeast cells expression of AtHSFA1d showed higher tolerance to HCHO stress than wild-type (WT) cells. AtHsfA1d was introduced into tobacco and the expression of AtHSFA1d in transgenic lines was demonstrated using Western blot analysis. Transgenic tobacco showed higher uptake rate to aqueous HCHO, had the higher biomass and produced higher content of total proteins than WT plants. These results indicated that AtHsfA1d conferred HCHO tolerance to yeast and tobacco. AtHsfA1d is a good candidate to develop phytoremediation plants for HCHO pollution.
Formaldehyde (HCHO) is highly toxic to all living organisms. In this study, the toxic effects of HCHO exposure on Arabidopsis thaliana were analyzed at the physiological and transcriptional levels. Exposure to 2 mM HCHO led to a significant decrease in plant growth and a massive increase in anthocyanin content. A remarkable increase in H₂O₂ content and elevation in the levels of protein carbonyl and DNA–protein crosslinks were detected in Arabidopsis plants exposed to 2 mM HCHO for a period of 17 h. In contrast, the malondialdehyde content decreased during this period. These results suggested that HCHO stress caused significant oxidative damage to proteins but not membrane lipids during this period. The Affymetrix ATH1 Genome Array was used to evaluate changes in the global gene expression in Arabidopsis plants exposed to 2 mM HCHO over the 17-h period. A total of 620 transcripts were shown to be regulated significantly (at least twofold). The number of down-regulated genes (467) was approximately threefold greater than the number of up-regulated genes (154). Down-regulation in a large number of genes encoding cell surface receptors, cell wall proteins, enzymes related to toxin metabolism, peroxidase, disease resistance protein, multidrug and toxin extrusion and ATP-binding cassette transporters might be an important part of the toxic effects of HCHO exposure on Arabidopsis at the transcriptional level. Up-regulation in many genes encoding heat shock proteins was suggested to be an important protective mechanism for Arabidopsis plants in response to the oxidative damage of proteins. Verification of microarray data by reverse transcription polymerase chain reaction analysis identified typical HCHO-induced and -repressed genes.
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