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      Hydrolytic and pumping activity of H+-ATPase from leaves of sugar beet (Beta vulgaris L.) as affected by salt stress

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      Journal of Plant Physiology
      Elsevier BV

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          Abstract

          Cell wall extensibility plays an important role in plant growth. According to the acid-growth theory, lower apoplastic pH allows extension growth by affecting cell wall extensibility. A lowered apoplastic pH is presumed to activate wall-loosening enzymes that control plant growth. Plasma membrane (PM) H(+)-ATPases play a major role in the apoplastic acidification by H(+) transport from cytosol to the apoplast. A salt-induced decrease in H(+)-pumping activity of plasma membrane H(+)-ATPases in salt-sensitive maize plants has previously been found. This led us to formulate the hypothesis that salt-resistant plant species such as sugar beet (Beta vulgaris L.) may have a mechanism to eliminate the effect of higher salt concentrations on plasma membrane H(+)-ATPase activity. In the present study, sugar beet plants were grown in 1mM NaCl (control) or 150 mM NaCl in hydroponics. H(+)-ATPase hydrolytic and pumping activities were measured in plasma membrane vesicles isolated from sugar beet shoots. We found that plasma membrane H(+)-ATPase hydrolytic and pumping activities were not affected by application of 150 mM NaCl. Moreover, apoplastic pH was also not affected under salt stress. However, a decrease in plant growth was observed. We assume that growth reduction was not due to a decrease in PM-H(+)-ATPase activity, but that other factors may be responsible for growth inhibition of sugar beet plants under salt stress.

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          Author and article information

          Journal
          Journal of Plant Physiology
          Journal of Plant Physiology
          Elsevier BV
          01761617
          June 2010
          June 2010
          : 167
          : 9
          : 725-731
          Article
          10.1016/j.jplph.2009.12.018
          20189265
          a1ebcb94-30a9-4ac5-8885-b63f0ed9dc45
          © 2010

          https://www.elsevier.com/tdm/userlicense/1.0/

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