Functional comparison of catalase genes in the elimination of photorespiratory H₂O₂ using promoter- and 3′-untranslated region exchange experiments in the Arabidopsis cat2 photorespiratory mutant

Photorespiration-associated production of H₂O₂ accounts for the majority of total H₂O₂ in leaves of C₃ plants and is mainly eliminated by catalases. In Arabidopsis, lack of CAT2, but not CAT1 or CAT3, results in growth suppression and a marked accumulation of H₂O₂ in leaves. To evaluate the contribu...

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Veröffentlicht in:Plant, cell and environment cell and environment, 2010-10, Vol.33 (10), p.1656-1670
Hauptverfasser: HU, YE-QIN, LIU, SHENG, YUAN, HONG-MEI, LI, JING, YAN, DA-WEI, ZHANG, JIAN-FENG, LU, YING-TANG
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Sprache:eng
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Zusammenfassung:Photorespiration-associated production of H₂O₂ accounts for the majority of total H₂O₂ in leaves of C₃ plants and is mainly eliminated by catalases. In Arabidopsis, lack of CAT2, but not CAT1 or CAT3, results in growth suppression and a marked accumulation of H₂O₂ in leaves. To evaluate the contribution of individual catalase genes and their promoters to catalase function, we investigated the growth suppression and H₂O₂ accumulation phenotypes of Arabidopsis derivatives expressing catalase genes from heterologous CAT promoters in a cat2 mutant background. The expression of CAT2 from the CAT2 promoter restored the wild-type phenotype in a cat2-1 mutant, while CAT1 and CAT3 promoter-driven expression of CAT2 did not. Ectopic expression of CAT3 from the CAT2 promoter also restored the normal phenotype, unlike that of CAT1 which required replacement of the CAT1 3′-untranslated region (UTR) with that of CAT2. These results demonstrated that the photorespiratory role of CAT2 is determined mainly by the regulation of its promoter activity. The 3′-UTR of CAT2 was vital for controlling CAT2 protein levels under photorespiratory conditions. Identification of component of heterotetramers catalase isoforms suggested that there is some functional redundancy between CAT2 and CAT1 and CAT3.
ISSN:0140-7791
1365-3040
DOI:10.1111/j.1365-3040.2010.02171.x