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Mol. Cells 2012; 34(3): 305-313

Published online September 6, 2012

https://doi.org/10.1007/s10059-012-0122-2

© The Korean Society for Molecular and Cellular Biology

ATAF2, a NAC Transcription Factor, Binds to the Promoter and Regulates NIT2 Gene Expression Involved in Auxin Biosynthesis

Sung Un Huh, Suk-Bae Lee, Hwang Hyun Kim, Kyung-Hee Paek*

School of Life Sciences and Biotechnology, Korea University, Seoul, 136-701, Korea

Correspondence to : *Correspondence: khpaek95@korea.ac.kr

Received: April 23, 2012; Revised: July 18, 2012; Accepted: July 18, 2012

Abstract

The transcription factor ATAF2, one of the plant specific NAC family genes, is known as repressor of pathogenesisrelated genes and responsive to the diverse defense-related hormones, pathogen infection, and wounding stress. Furthermore, it is important to consider that tryptophandependant IAA biosynthesis pathway can be activated by wounding and pathogen. We found that ATAF2pro::GUS reporter was induced upon indole-3-acetonitrile (IAN) treatments. And ataf2 mutant showed reduced sensitivity to IAN whereas 35S::ATAF2 plants showed hyper-sensitivity to IAN. IAN biosynthesis required nitrilase involved in the conversion of IAN to an auxin, indole-3-acetic acid (IAA). We found that the NIT2 gene was repressed in ataf2 knockout plants. Expression of both ATAF2 and NIT2 genes was induced by IAN treatment. Transgenic plants overexpressing ATAF2 showed up-regulated NIT2 expression. ATAF2 activated promoter of the NIT2 gene in Arabidopsis protoplasts. Electrophoretic mobility shift assay revealed that NIT2 promoter region from position -117 to -82 contains an ATAF2 binding site where an imperfect palindrome sequence was critical to the protein-DNA interaction. These findings indicate that ATAF2 regulates NIT2 gene expression via NIT2 promoter binding.

Keywords Arabidopsis, ATAF2, Auxin, NAC transcription factor, Nitrilase

Article

Research Article

Mol. Cells 2012; 34(3): 305-313

Published online September 30, 2012 https://doi.org/10.1007/s10059-012-0122-2

Copyright © The Korean Society for Molecular and Cellular Biology.

ATAF2, a NAC Transcription Factor, Binds to the Promoter and Regulates NIT2 Gene Expression Involved in Auxin Biosynthesis

Sung Un Huh, Suk-Bae Lee, Hwang Hyun Kim, Kyung-Hee Paek*

School of Life Sciences and Biotechnology, Korea University, Seoul, 136-701, Korea

Correspondence to:*Correspondence: khpaek95@korea.ac.kr

Received: April 23, 2012; Revised: July 18, 2012; Accepted: July 18, 2012

Abstract

The transcription factor ATAF2, one of the plant specific NAC family genes, is known as repressor of pathogenesisrelated genes and responsive to the diverse defense-related hormones, pathogen infection, and wounding stress. Furthermore, it is important to consider that tryptophandependant IAA biosynthesis pathway can be activated by wounding and pathogen. We found that ATAF2pro::GUS reporter was induced upon indole-3-acetonitrile (IAN) treatments. And ataf2 mutant showed reduced sensitivity to IAN whereas 35S::ATAF2 plants showed hyper-sensitivity to IAN. IAN biosynthesis required nitrilase involved in the conversion of IAN to an auxin, indole-3-acetic acid (IAA). We found that the NIT2 gene was repressed in ataf2 knockout plants. Expression of both ATAF2 and NIT2 genes was induced by IAN treatment. Transgenic plants overexpressing ATAF2 showed up-regulated NIT2 expression. ATAF2 activated promoter of the NIT2 gene in Arabidopsis protoplasts. Electrophoretic mobility shift assay revealed that NIT2 promoter region from position -117 to -82 contains an ATAF2 binding site where an imperfect palindrome sequence was critical to the protein-DNA interaction. These findings indicate that ATAF2 regulates NIT2 gene expression via NIT2 promoter binding.

Keywords: Arabidopsis, ATAF2, Auxin, NAC transcription factor, Nitrilase

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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