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Mol. Cells 2004; 18(2): 207-213

Published online January 1, 1970

© The Korean Society for Molecular and Cellular Biology

Pathogenesis-related Gene Expression by Specific Calmodulin Isoforms Is Dependent on NIM1, a Key Regulator of Systemic Acquired Resistance

Chan Young Park, Won Do Heo, Jae Hyuk Yoo, Ju Huck Lee, Min Chul Kim, Hyun Jin Chun, Byeong Cheol Moon, Ihn Hyeong Kim, Hyeong Cheol Park, Man Soo Choi, Hyun Mi Ok, Mi Sun Cheong, Sang Min Lee, Ho Soo Kim, Kon Ho Lee, Chae Oh Lim, Woo Sik Chung, Moo Je Cho

Abstract

Plants produce numerous calmodulin isoforms that exhibit differential gene expression patterns and sense different Ca2+ signals. This diversity results in different physiological responses to particular stimuli. Gm-CaM-4 and -5 are two divergent calmodulin isoforms from the soybean (Glycine max) that have been reported to be involved in plant disease resistance. However, little is known about the pathway by which these specific isoforms transduce the defense signal and up-regulate pathogenesis-related (PR) genes. Here we report that overexpression of GmCaM-4/-5 induces constitutive PR gene expression and enhances disease resistance in wild-type Arabidopsis, but not in the nim1 mutant of Arabidopsis. GmCaM-4/-5 also appear to activate trans-acting elements that bind to cis-acting elements in the Arabidopsis PR-1 promoter. Thus up-regulation of PR genes by these GmCaM isoforms is dependent on NIM1 (Non immunity 1) and unknown transcription factors.

Keywords Arabidopsis; Calmodulin; NIM1; Plant Defense; PR Gene

Article

Research Article

Mol. Cells 2004; 18(2): 207-213

Published online October 31, 2004

Copyright © The Korean Society for Molecular and Cellular Biology.

Pathogenesis-related Gene Expression by Specific Calmodulin Isoforms Is Dependent on NIM1, a Key Regulator of Systemic Acquired Resistance

Chan Young Park, Won Do Heo, Jae Hyuk Yoo, Ju Huck Lee, Min Chul Kim, Hyun Jin Chun, Byeong Cheol Moon, Ihn Hyeong Kim, Hyeong Cheol Park, Man Soo Choi, Hyun Mi Ok, Mi Sun Cheong, Sang Min Lee, Ho Soo Kim, Kon Ho Lee, Chae Oh Lim, Woo Sik Chung, Moo Je Cho

Abstract

Plants produce numerous calmodulin isoforms that exhibit differential gene expression patterns and sense different Ca2+ signals. This diversity results in different physiological responses to particular stimuli. Gm-CaM-4 and -5 are two divergent calmodulin isoforms from the soybean (Glycine max) that have been reported to be involved in plant disease resistance. However, little is known about the pathway by which these specific isoforms transduce the defense signal and up-regulate pathogenesis-related (PR) genes. Here we report that overexpression of GmCaM-4/-5 induces constitutive PR gene expression and enhances disease resistance in wild-type Arabidopsis, but not in the nim1 mutant of Arabidopsis. GmCaM-4/-5 also appear to activate trans-acting elements that bind to cis-acting elements in the Arabidopsis PR-1 promoter. Thus up-regulation of PR genes by these GmCaM isoforms is dependent on NIM1 (Non immunity 1) and unknown transcription factors.

Keywords: Arabidopsis, Calmodulin, NIM1, Plant Defense, PR Gene

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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