These authors contributed equally to this work.
Uncoupling phosphate deficiency from its major effects on growth and transcriptome via PHO1 expression in Arabidopsis
Article first published online: 2 FEB 2011
© 2011 The Authors. The Plant Journal © 2011 Blackwell Publishing Ltd
The Plant Journal
Volume 65, Issue 4, pages 557–570, February 2011
How to Cite
Rouached, H., Stefanovic, A., Secco, D., Bulak Arpat, A., Gout, E., Bligny, R. and Poirier, Y. (2011), Uncoupling phosphate deficiency from its major effects on growth and transcriptome via PHO1 expression in Arabidopsis. The Plant Journal, 65: 557–570. doi: 10.1111/j.1365-313X.2010.04442.x
- Issue published online: 2 FEB 2011
- Article first published online: 2 FEB 2011
- Accepted manuscript online: 29 NOV 2010 12:00AM EST
- Received 8 September 2010; revised 22 October 2010; accepted 24 November 2010.
- nutrient deficiency;
- signal transduction
Inorganic phosphate (Pi) is one of the most limiting nutrients for plant growth in both natural and agricultural contexts. Pi-deficiency leads to a strong decrease in shoot growth, and triggers extensive changes at the developmental, biochemical and gene expression levels that are presumably aimed at improving the acquisition of this nutrient and sustaining growth. The Arabidopsis thaliana PHO1 gene has previously been shown to participate in the transport of Pi from roots to shoots, and the null pho1 mutant has all the hallmarks associated with shoot Pi deficiency. We show here that A. thaliana plants with a reduced expression of PHO1 in roots have shoot growth similar to Pi-sufficient plants, despite leaves being strongly Pi deficient. Furthermore, the gene expression profile normally triggered by Pi deficiency is suppressed in plants with low PHO1 expression. At comparable levels of shoot Pi supply, the wild type reduces shoot growth but maintains adequate shoot vacuolar Pi content, whereas the PHO1 underexpressor maintains maximal growth with strongly depleted Pi reserves. Expression of the Oryza sativa (rice) PHO1 ortholog in the pho1 null mutant also leads to plants that maintain normal growth and suppression of the Pi-deficiency response, despite the low shoot Pi. These data show that it is possible to unlink low shoot Pi content with the responses normally associated with Pi deficiency through the modulation of PHO1 expression or activity. These data also show that reduced shoot growth is not a direct consequence of Pi deficiency, but is more likely to be a result of extensive gene expression reprogramming triggered by Pi deficiency.