|Tian, Hui -|
|Lahner, Brett -|
|Salt, David -|
|Ward, John -|
Submitted to: The Plant Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: December 11, 2010
Publication Date: December 30, 2010
Citation: Tian, H., Baxter, I.R., Lahner, B., Salt, D.E., Ward, J.M. 2010. Arabidopsis AtNaKR1 is a phloem mobile metal-binding protein necessary for phloem function and root meristem maintenance. The Plant Cell. 22:3963-3979. Interpretive Summary: A major problem for world agriculture is the growing decrease in available arable land. More and more we are working in soils that impart a stress on the plants that make up the crops we depend on. In order for plants to survive without being able to move out of unfavorable soil environments, they adjust the biochemical composition of their tissues through a wide variety of mechanisms. One of these mechanisms is to move elements such as sodium (Na) and potassium (K) from tissue to tissue, including from the root to the shoot and back again. Understanding the molecular basis of these mechanisms will enable the production of crops that are better able to respond to the changing environment and increase yields with fewer inputs. In this study, we identified and characterized a gene which is important for loading Na into the phloem, the 'veins' of the plant responsible for moving molecules out of the leaves to the seeds and roots. The protein also moves into the phloem. Plants without a functional form of this gene, called NAKR1, have altered levels of Na, K and starch in the leaves, have shorter roots and flower later than plants with a functional copy of NAKR1. These results will lead to a better understanding of how plants distribute elements between tissues and ultimately will allow for crop improvement strategies that deal with poor soil quality.
Technical Abstract: The SODIUM POTASSIUM ROOT DEFECTIVE 1 (NaKR1) encodes a soluble metal binding protein that is specifically expressed in companion cells of the phloem. The nakr1-1 mutant phenotype includes high Na+, K+, and Rb+ accumulation in leaves, short roots, and late flowering. Starch accumulation in the leaves of the mutant was also consistent with defective function on the phloem. Using traditional and DNA microarray-based mapping, a 7 bp deletion was found in an exon of NaKR1 that caused a premature stop. The mutant phenotypes were complemented by the native gene and by GFP and GUS fusions driven by the native promoter. NAKR1-GFP was mobile in the phloem, it moved into sieve elements and into a novel symplasmic domain of the root meristem. Grafting experiments revealed that the high Na+ accumulation was due to loss of NaKR1 function in the leaves. This supports a role for the phloem in recirculating Na+ to the roots to provide Na+ homeostasis. The onset of root phenotypes coincided with NaKR1 expression after germination. Short root length was primarily due to a decrease in cell division rate in the root meristem indicating a role for NaKR1 expression in the phloem in root meristem maintenance.