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Title

Computational predictions of common transcription factor binding sites on the genes of proline metabolism in plants

 

Authors

Usha Kiran1 & Malik Zainul Abdin2*

 

Affiliation

1Faculty of Interdisciplinary Research Studies, Jamia Hamdard, New Delhi-110062, India; 2Department of Biotechnology, Faculty of Science, Jamia Hamdard, New Delhi-110062, India

 

Email

mzabdin@rediffmail.com; *Corresponding author

 

Article Type

Hypothesis

 

Date

Received August 22, 2012; Accepted September 03, 2012; Published September 21, 2012

Abstract

Proline, an imino acid, has been well documented to be associated with the stress response induced by abiotic factors such as drought, cold and salinity in plants and biotic factors such as bacterial and fungal attacks. However, the regulatory mechanisms controlling proline metabolism, intercellular and intracellular transport and connections of proline to other metabolic pathways are poorly understood. F-MATCH analysis combined with composite module analysis (CMA) revealed that the binding sites matching matrices for O2 and OCSBF-1 were overrepresented in the promoters of differentially expressed proline metabolism genes. The presence of MYBAS1 consensus binding sites occurring in combination with O2 and OCSBF1 in the promoters of genes of proline biosynthesis pathway and SBF1 and GT1 consensus binding sites occurring in combination with O2 and OCSBF1 in the promoters of proline catabolic pathway genes suggest their involvement in modulation of proline metabolism and its accumulation in plants.

 

Keywords

Proline, stress, composite module analysis, promoter, transcription factor binding sites

 

Citation

Kiran & Abdin, Bioinformation 8(18): 886-890 (2012)

Edited by

P Kangueane

 

ISSN

0973-2063

 

Publisher

Biomedical Informatics

 

License

This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.