A role for HKT1 in sodium uptake by wheat roots

A - Papers appearing in refereed journals

Laurie, S., Feeney, K. A., Maathuis, F. J. M., Heard, P. J., Brown, S. J. and Leigh, R. A. 2002. A role for HKT1 in sodium uptake by wheat roots. The Plant Journal. 32 (2), pp. 139-149. https://doi.org/10.1046/j.1365-313X.2002.01410.x

AuthorsLaurie, S., Feeney, K. A., Maathuis, F. J. M., Heard, P. J., Brown, S. J. and Leigh, R. A.

The high affinity potassium transporter, HKT1 from wheat was introduced into Florida wheat in sense and antisense orientation under control of a ubiquitin promoter. Ten transgenic lines expressing the transgene were identified and two of these showed strong down-regulation of the native HKT1 transcript. One line (271) was expressing the antisense construct and the other (223) was expressing a truncated sense construct. The two lines were examined further for phenotype relating to cation transport. Membrane depolarisations were measured in low (0.1 mm) K+ and high (100 mm) NaCl. Under these conditions there was no difference between line 271 and the control at low K+, but at high Na+ there was a rapid depolarisation that was significantly larger in control plants. Na-22 uptake was measured in this line and there was a significant decrease in uptake at 100 mm NaCl in the transgenic line when compared with the control. The two transgenic lines were grown at high NaCl (200 mm) and analysed for growth and root sodium content. Lines 271 and 223 showed enhanced growth under salinity when compared with the control and had lower sodium in the root. Secondary ion mass spectrometry (SIMS) analysis of transverse sections of the root showed that Na+ and K+ were strongly localised to stelar regions when compared with other ions, and that the Na+:K+ ratios were reduced in salt-stressed transgenic tissue when compared with the control.

KeywordsPlant Sciences
Year of Publication2002
JournalThe Plant Journal
Journal citation32 (2), pp. 139-149
Digital Object Identifier (DOI)https://doi.org/10.1046/j.1365-313X.2002.01410.x
PubMed ID12383080
Open accessPublished as non-open access
Funder project or code414

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