Publication Type: | Journal Article |
Year of Publication: | 2010 |
Authors: | Tian, H, Baxter, IR, Lahner, B, Reinders, A, Salt, DE, Ward, JM |
Journal: | The Plant Cell |
Volume: | 22 |
Issue: | 12 |
Date Published: | 2010 |
ISBN Number: | 10404651 |
Abstract: | SODIUM POTASSIUM ROOT DEFECTIVE1 (NaKR1; previously called NPCC6) 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⁺, Rb⁺, and starch accumulation in leaves, short roots, late flowering, and decreased long-distance transport of sucrose. Using traditional and DNA microarray-based deletion mapping, a 7-bp deletion was found in an exon of NaKR1 that introduced a premature stop codon. The mutant phenotypes were complemented by transformation with the native gene or NaKR1-GFP (green fluorescent protein) and NaKR1-β-glucuronidase fusions driven by the native promoter. NAKR1-GFP was mobile in the phloem; it moved from companion cells into sieve elements and into a previously undiscovered symplasmic domain in the root meristem. Grafting experiments revealed that the high Na⁺ accumulation was due mainly to loss of NaKR1 function in the leaves. This supports a role for the phloem in recirculating Na⁺ to the roots to limit Na⁺ accumulation in leaves. The onset of root phenotypes coincided with NaKR1 expression after germination. The nakr1-1 short root phenotype was due primarily to a decreased cell division rate in the root meristem, indicating a role in root meristem maintenance for NaKR1 expression in the phloem. |
URL: | http://www.jstor.org/stable/41059406 |
Short Title: | The Plant Cell |