Arabidopsis NPCC6/NaKR1 Is a Phloem Mobile Metal Binding Protein Necessary for Phloem Function and Root Meristem Maintenance

Hui Tian, Ivan R. Baxter, Brett Lahner, Anke Reinders, David E. Salt, John M. Ward

Research output: Contribution to journalArticle

34 Citations (Scopus)

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-beta-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.

Original languageEnglish
Pages (from-to)3963-3979
Number of pages17
JournalThe Plant Cell
Volume22
Issue number12
DOIs
Publication statusPublished - Dec 2010

Keywords

  • localized K+ channel
  • intercellular transport
  • dependent regulation
  • floral induction
  • companion cells
  • salt tolerance
  • messenger-RNA
  • FT protein
  • ATX1 gene
  • thaliana

Cite this

Arabidopsis NPCC6/NaKR1 Is a Phloem Mobile Metal Binding Protein Necessary for Phloem Function and Root Meristem Maintenance. / Tian, Hui; Baxter, Ivan R.; Lahner, Brett; Reinders, Anke; Salt, David E.; Ward, John M.

In: The Plant Cell, Vol. 22, No. 12, 12.2010, p. 3963-3979.

Research output: Contribution to journalArticle

Tian, Hui ; Baxter, Ivan R. ; Lahner, Brett ; Reinders, Anke ; Salt, David E. ; Ward, John M. / Arabidopsis NPCC6/NaKR1 Is a Phloem Mobile Metal Binding Protein Necessary for Phloem Function and Root Meristem Maintenance. In: The Plant Cell. 2010 ; Vol. 22, No. 12. pp. 3963-3979.
@article{7f5d3a498a1f4f6da2ca3c1dadadd9d5,
title = "Arabidopsis NPCC6/NaKR1 Is a Phloem Mobile Metal Binding Protein Necessary for Phloem Function and Root Meristem Maintenance",
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-beta-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.",
keywords = "localized K+ channel, intercellular transport, dependent regulation, floral induction, companion cells, salt tolerance, messenger-RNA, FT protein, ATX1 gene, thaliana",
author = "Hui Tian and Baxter, {Ivan R.} and Brett Lahner and Anke Reinders and Salt, {David E.} and Ward, {John M.}",
year = "2010",
month = "12",
doi = "10.1105/tpc.110.080010",
language = "English",
volume = "22",
pages = "3963--3979",
journal = "The Plant Cell",
issn = "1040-4651",
publisher = "American Society of Plant Biologists",
number = "12",

}

TY - JOUR

T1 - Arabidopsis NPCC6/NaKR1 Is a Phloem Mobile Metal Binding Protein Necessary for Phloem Function and Root Meristem Maintenance

AU - Tian, Hui

AU - Baxter, Ivan R.

AU - Lahner, Brett

AU - Reinders, Anke

AU - Salt, David E.

AU - Ward, John M.

PY - 2010/12

Y1 - 2010/12

N2 - 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-beta-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.

AB - 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-beta-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.

KW - localized K+ channel

KW - intercellular transport

KW - dependent regulation

KW - floral induction

KW - companion cells

KW - salt tolerance

KW - messenger-RNA

KW - FT protein

KW - ATX1 gene

KW - thaliana

U2 - 10.1105/tpc.110.080010

DO - 10.1105/tpc.110.080010

M3 - Article

VL - 22

SP - 3963

EP - 3979

JO - The Plant Cell

JF - The Plant Cell

SN - 1040-4651

IS - 12

ER -