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The promoter of the pepper pathogen-induced membrane protein gene CaPIMP1 mediates environmental stress responses in plants

Authors
Hong, Jeum KyuHwang, Byung Kook
Issue Date
1월-2009
Publisher
SPRINGER
Keywords
Capsicum annuum; Osmotic stress; Oxidative damage; Plasma membrane protein; Promoter activation; Transgenic Arabidopsis
Citation
PLANTA, v.229, no.2, pp.249 - 259
Indexed
SCIE
SCOPUS
Journal Title
PLANTA
Volume
229
Number
2
Start Page
249
End Page
259
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/120863
DOI
10.1007/s00425-008-0824-z
ISSN
0032-0935
Abstract
The promoter of the pepper pathogen-induced membrane protein gene CaPIMP1 was analyzed by an Agrobacterium-mediated transient expression assay in tobacco leaves. Several stress-related cis-acting elements (GT-1, W-box and ABRE) are located within the CaPIMP1 promoter. In tobacco leaf tissues transiently transformed with a CaPIMP1 promoter-beta-glucuronidase (GUS) gene fusion, serially 5'-deleted CaPIMP1 promoters were differentially activated by Pseudomonas syringae pv. tabaci, ethylene, methyl jasmonate, abscisic acid, and nitric oxide. The -1,193 bp region of the CaPIMP1 gene promoter sequence exhibited full promoter activity. The -417- and -593 bp promoter regions were sufficient for GUS gene activation by ethylene and methyl jasmonate treatments, respectively. However, CaPIMP1 promoter sequences longer than -793 bp were required for promoter activation by abscisic acid and sodium nitroprusside treatments. CaPIMP1 expression was activated in pepper leaves by treatment with ethylene, methyl jasmonate, abscisic acid, beta-amino-n-butyric acid, NaCl, mechanical wounding, and low temperature, but not with salicylic acid. Overexpression of CaPIMP1 in Arabidopsis conferred hypersensitivity to mannitol, NaCl, and ABA during seed germination but not during seedling development. In contrast, transgenic plants overexpressing CaPIMP1 exhibited enhanced tolerance to oxidative stress induced by methyl viologen during germination and early seedling stages. These results suggest that CaPIMP1 expression may alter responsiveness to environmental stress, as well as to pathogen infection.
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