Format

Send to:

Choose Destination
See comment in PubMed Commons below
Plant Cell Environ. 2014 Jul;37(7):1586-97. doi: 10.1111/pce.12258. Epub 2014 Mar 20.

Identification of early Al-responsive genes in rice bean (Vigna umbellata) roots provides new clues to molecular mechanisms of Al toxicity and tolerance.

Author information

  • 1State Key Laboratory of Plant Physiology and Biochemistry, College of Life Sciences, Zhejiang University, Hangzhou, 310058, China.

Abstract

Significant secretion of citrate from root apex of rice bean (Vigna umbellata) is delayed by several hours under aluminium (Al) stress. However, the molecular basis of regulation of VuMATE1, a gene encoding an Al-activated citrate transporter, remains unclear. In this study, we used suppression subtractive hybridization together with reverse northern blot analysis and qRT-PCR to identify genes with altered transcript levels in the root apex after treatment with low (5 μm) or high (25 μm) concentration of AlCl(3) for a short time (4 h). We found that in addition to VuMATE1, 393 genes showed an early response to Al. Among functionally annotated genes, those related to 'metabolism and energy', 'signal transduction and transcription' and 'transport' was predominantly up-regulated, whereas those associated with 'protein translation, processing and degradation' was predominantly down-regulated. Comparative analysis of transcriptional profiles highlighted candidate genes associated with citrate secretion and revealed several new aspects of the molecular processes underlying Al toxicity and tolerance. Based on the data, it is proposed that metabolic changes represent adaptive mechanisms to Al stress, whereas inhibition of both cell elongation and cell division underlies Al-induced root growth inhibition.

© 2013 John Wiley & Sons Ltd.

KEYWORDS:

aluminium stress; cell wall; citrate secretion; metabolism; signal transduction; suppression subtractive hybridization

PMID:
24372448
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Blackwell Publishing
    Loading ...
    Write to the Help Desk