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Molecular characterization of a novel AP2 transcription factor ThWIND1-L from Thellungiella halophila

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Abstract

Several AP2/ERF transcription factors are wound-induced regulators, which play key roles in controlling cell dedifferentiation. In this study, a novel AP2/ERF transcription factor, the WIND1-like gene (ThWIND1-L), was isolated and characterized from Thellungiella halophila. ThWIND1-L cDNA clone contained a full open reading frame (ORF) of 1,068 bp encoding 356 amino acids. The predicted amino acid sequence of ThWIND1-L cDNA shared remarkably high degree of identity with the Arabidopsis RAP2.4 (WIND1). The expression of ThWIND1-L rapidly responded to the wound signals, ectopic expression of ThWIND1-L in Arabidopsis plants promoted callus tissue formation without the presence of exogenous hormones. Furthermore, overexpression of ThWIND1-L influenced some primary transcription factors (TFs), which have been shown to be involved in cell dedifferentiation and shoot regeneration. These results indicated ThWIND1-L might be a wound-induced regulator, which played an important role in the control of cell dedifferentiation.

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Abbreviations

TFs:

Transcription factors

ORF:

Open reading frame

RACE:

Rapid amplification of cDNA ends

SAM:

Shoot apical meristem

2,4-D:

2,4-Dichlorophenoxyacetic acid

EST:

Expressed sequence tag

OE-ThWIND1-L :

Overexpression of ThWIND1-L

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Acknowledgments

Our work was supported by the National Natural Science Foundation of China (grant no. 30970169).

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Authors and Affiliations

  1. Department of Molecular and Cell Biology, School of Life Science and Technology, Tongji University, 200092, Shanghai, China

    Cheng Zhou, Jiansheng Guo, Zhenhua Feng, Xianghuan Cui & Jian Zhu

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  1. Cheng Zhou
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  2. Jiansheng Guo
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  3. Zhenhua Feng
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  4. Xianghuan Cui
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  5. Jian Zhu
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Correspondence to Jian Zhu.

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Zhou, C., Guo, J., Feng, Z. et al. Molecular characterization of a novel AP2 transcription factor ThWIND1-L from Thellungiella halophila . Plant Cell Tiss Organ Cult 110, 423–433 (2012). https://doi.org/10.1007/s11240-012-0163-4

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  • DOI: https://doi.org/10.1007/s11240-012-0163-4

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