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The HKT Transporter Gene from Arabidopsis, AtHKT1;1, Is Dominantly Expressed in Shoot Vascular Tissue and Root Tips and Is Mild Salt Stress-Responsive
The Arabidopsis high-affinity K(+) transporter (AtHKT1;1) plays roles in salt tolerance by unloading Na(+) from the root xylem to the xylem parenchyma cells and/or uploading Na(+) from the shoot/leaf xylem to the xylem parenchyma cells. To use this promoter for the molecular breeding of salt-toleran...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6681212/ https://www.ncbi.nlm.nih.gov/pubmed/31277362 http://dx.doi.org/10.3390/plants8070204 |
Sumario: | The Arabidopsis high-affinity K(+) transporter (AtHKT1;1) plays roles in salt tolerance by unloading Na(+) from the root xylem to the xylem parenchyma cells and/or uploading Na(+) from the shoot/leaf xylem to the xylem parenchyma cells. To use this promoter for the molecular breeding of salt-tolerant plants, I evaluated the expression profile of the AtHKT1;1 promoter in detail. Approximately 1.1 kbp of sequence upstream from the start codon of AtHKT1;1 was polymerase chain reaction (PCR)-amplified, fused to the β-glucuronidase (GUS) gene, and introduced into Arabidopsis. The resultant transformants were evaluated under nonstressed and salt-stress conditions at the seedling and reproductive stages. Histochemical analysis showed that GUS activity was detected in vascular bundle tissue in roots, hypocotyls, petioles, leaves, and petals, and in root tips. GUS enzyme activity in shoots tended to be higher than that in roots at both stages. After treatment with 50 mM NaCl for 24 h, GUS transcription levels and GUS enzyme activity were enhanced in transgenic lines. These results indicate that the AtHKT1;1 promoter isolated in this study could be useful in expressing transgenes specifically in vascular tissue and root tips, and in a mild salt-stress-responsive manner. The data provide novel insights into the functions of AtHKT1;1. |
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