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GST成員參與阿拉伯芥光訊息傳遞的研究
Studies of the involvment of glutathione S-transferases in light signal transduction in Arabidopsis thaliana
Date Issued
2006
Date
2006
Author(s)
Liu, Ming-Jung
DOI
en-US
Abstract
Previous studies have shown that a glutathione S-transferase (GST), a tau class member of the GST gene family in Arabidopsis, can interact with the C-terminus of FIN219 that functions as a positive regulator of phytochrome A (phyA)-mediated far-red (FR) light signaling. Tepperman et al. (2001) reported that a GST (AtGSTU17) mRNA expression was induced rapidly in wild type under FR light, but abolished in the phyA mutant.
To further investigate whether some GST members will be involved in photomorphogenesis, we analyzed the AtGSTU17 transcript under FR condition. Northern blotting analyses showed that AtGSTU17 expression was indeed induced by FR and regulated by PHYA. Moreover, its expression was light intensity-dependent. Purified recombinant protein AtGSTU17 also showed GST activities with both substrates glutathione (GSH) and 1-chloro-2,4-dinitrobenzene (CDNB). Furthermore, transgenic seedlings overexpressing AtGSTU17 exhibited a hypersensitive phenotype under FR, whereas the knock-out mutant of AtGSTU17 (atgstu17) showed a longer hypocotyl phenotype compared to wild type. In addition, transgenic seedlings overexpressing or inhibiting AtGSTU17 expression also affected FR-mediated anthocyanin accumulation and chlorophyll killing. Moreover, atgstu17 mutants displayed a delayed flowering phenotype under long-day condition. In contrast, 35S:AtGSTU17 transgenic plants exhibited slightly earlier flowering under the same condition. Genetic analysis indicated that PHYA and ATGSTU17 appeared to show a relationship of nonallelic noncomplementation. Promoter activity assays revealed that AtGSTU17 was mainly expressed in vascular tissues of the seedlings and floral organs.
As well, AtGSTU17 was induced by several hormones, such as ABA, 2,4-D, and JA. Intriguingly, atgstu17 seedlings displayed insensitivity to ABA-mediated inhibition of root elongation, whereas, 35S:AtGSTU17 transgenic plants showed almost equal sensitivity to exogenous ABA effect.
Taken together, our data indicate AtGSTU17 may function as a crosstalk between FR light and multiple hormones to regulate hypocotyl elongation and root growth.
To further investigate whether some GST members will be involved in photomorphogenesis, we analyzed the AtGSTU17 transcript under FR condition. Northern blotting analyses showed that AtGSTU17 expression was indeed induced by FR and regulated by PHYA. Moreover, its expression was light intensity-dependent. Purified recombinant protein AtGSTU17 also showed GST activities with both substrates glutathione (GSH) and 1-chloro-2,4-dinitrobenzene (CDNB). Furthermore, transgenic seedlings overexpressing AtGSTU17 exhibited a hypersensitive phenotype under FR, whereas the knock-out mutant of AtGSTU17 (atgstu17) showed a longer hypocotyl phenotype compared to wild type. In addition, transgenic seedlings overexpressing or inhibiting AtGSTU17 expression also affected FR-mediated anthocyanin accumulation and chlorophyll killing. Moreover, atgstu17 mutants displayed a delayed flowering phenotype under long-day condition. In contrast, 35S:AtGSTU17 transgenic plants exhibited slightly earlier flowering under the same condition. Genetic analysis indicated that PHYA and ATGSTU17 appeared to show a relationship of nonallelic noncomplementation. Promoter activity assays revealed that AtGSTU17 was mainly expressed in vascular tissues of the seedlings and floral organs.
As well, AtGSTU17 was induced by several hormones, such as ABA, 2,4-D, and JA. Intriguingly, atgstu17 seedlings displayed insensitivity to ABA-mediated inhibition of root elongation, whereas, 35S:AtGSTU17 transgenic plants showed almost equal sensitivity to exogenous ABA effect.
Taken together, our data indicate AtGSTU17 may function as a crosstalk between FR light and multiple hormones to regulate hypocotyl elongation and root growth.
Subjects
阿拉伯芥
光型態發生
GST
PHOTOMORPHOGENESIS
Type
other
File(s)
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ntu-95-R93b42011-1.pdf
Size
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Format
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Checksum
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