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Function of NHX-type transporters in improving rice tolerance to aluminum stress and soil acidity

Li, W, Du, J, Feng, H, Wu, Q, Xu, G, Shabala, S ORCID: 0000-0003-2345-8981 and Yu, L 2020 , 'Function of NHX-type transporters in improving rice tolerance to aluminum stress and soil acidity' , Planta, vol. 251, no. 3 , pp. 1-13 , doi: 10.1007/s00425-020-03361-x.

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Abstract

Plant sodium (potassium)/proton (Na+(K+)/H+ antiporters of the NHX family have been extensively characterized as they are related to the enhancement of salt tolerance. However, no previous study has reported NHX transporter functions in plant tolerance to Al3+ toxicity. In this study, we demonstrate their role as a component of the Al3+ stress tolerance mechanism. We show that the ectopic expression of either HtNHX1 or HtNHX2 , from Helianthus tuberosus plant, in rice (located at vacuole and endosome, respectively) could also enhance rice tolerance to Al3+ stress and soil acidity. Expression of either HtNHX1 or HtNHX2 reduced the inhibitory effect of Al3+ on the rice root elongation rate; both genes were reported to be equally effective in improvement of stress conditions. Expression of HtNHX1 enhanced Al3+-trigged-secretion of citrate acids, rhizosphere acidification, and also reduced K+ efflux from root tissues. In contrast, expression of HtNHX2 prevented Al3+-trigged-decrease of H+ influx into root tissues. Al3+-induced damage of the cell wall extensibility at the root tips was impaired by either HtNHX1 or HtNHX2. Co-expression of HtNHX1 and HtNHX2 further improved rice growth, particularly under the Al3+ stress conditions. The results demonstrate that HtNHX1 and HtNHX2 improved rice tolerance to Al3+ via different mechanisms by altering the K+ and H+ fluxes and the cell wall structure.

Item Type: Article
Authors/Creators:Li, W and Du, J and Feng, H and Wu, Q and Xu, G and Shabala, S and Yu, L
Keywords: aluminum stress, endosome, K+(H+) fluxes, Na+(K+)/H+ antiporters, rice, vacuole, NHX, vacuole, acid soil
Journal or Publication Title: Planta
Publisher: Springer-Verlag
ISSN: 0032-0935
DOI / ID Number: 10.1007/s00425-020-03361-x
Copyright Information:

Copyright 2020 Springer-Verlag GmbH Germany, part of Springer Nature

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