Article ID Journal Published Year Pages File Type
5515404 Plant Physiology and Biochemistry 2017 10 Pages PDF
Abstract

•Salt tolerance in Sesuvium portulacastrum due to both succulence and bladder cells.•Cadmium delays upregulation of AHA1 and SOS1 under salt stress.•Cadmium increases cytoplasmic Na+ in salt exposed S. portulacastrum.•Enhanced BADH expression due to Cd-induced osmotic stress.

It is well known that salinity reduces cadmium toxicity in halophytes. However, the possible interference of Cd with the mechanisms of salt tolerance is poorly explored. The aim of this study was to see whether Cd affects salt tolerance mechanisms in the halophyte Sesuvium portulacastrum. S. portulacastrum plants obtained from cuttings were grown in hydroponics for 3 weeks and then exposed to low (0.09 mM) or moderate (200 mM) NaCl concentrations, alone or in combination with 25 μM CdCl2. Microscopy observation revealed two strategies of salt tolerance: euhalophytism and secretion of salt by bladder cells. Cadmium exposure hardly influenced the total leaf Na+ concentrations. However, Cd supply delayed the salt-induced upregulation of AHA1 (plasma membrane H+-ATPase 1) and SOS1 (plasma membrane Na+ transporter “Salt Overly Sensitive 1”), genes that are essential for salt tolerance. Moreover, Cd induced the activation of BADH, coding for betaine aldehyde dehydrogenase, indicating enhanced osmotic stress due to Cd. Sodium-green fluorescence in protoplasts from plants grown with low or high NaCl, alone or in combination with Cd, revealed higher Na+ concentrations in the cytoplasm of Cd-exposed plants. Taken together the results indicate interference of Cd with salt tolerance mechanisms in S. portulacastrum. This may have consequences for the efficient use of halophytes in phytoremediation of Cd-contaminated saline soils.

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