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Influence of sulfate supply on selenium uptake dynamics and expression of sulfate/selenate transporters in selenium hyperaccumulator and nonhyperaccumulator Brassicaceae
Author(s) -
El Mehdawi Ali F.,
Jiang Ying,
Guignardi Zack S.,
Esmat Ahmad,
Pilon Marinus,
PilonSmits Elizabeth A. H.,
Schiavon Michela
Publication year - 2018
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.14838
Subject(s) - selenate , sulfate , selenium , hyperaccumulator , chemistry , brassica , chromosomal translocation , shoot , biochemistry , sulfur , transporter , botany , environmental chemistry , biology , phytoremediation , gene , heavy metals , organic chemistry
SummaryStanleya pinnata not only hyperaccumulates selenium (Se) to 0.5% of its dry weight, but also exhibits higher tissue Se‐to‐sulfur (S) ratios than other species and its surroundings. To investigate the mechanisms underlying this Se enrichment, we compared S. pinnata with the nonhyperaccumulators S. elata and Brassica juncea for selenate uptake in long‐ (9 d) and short‐term (1 h) assays, using different concentrations of selenate and competitor sulfate. Different sulfate pre‐treatments (0, 0.5, 5 mM, 3 d) were also tested for effects on selenate uptake and sulfate transporters’ expression. Relative to nonhyperaccumulators, S. pinnata showed higher rates of root and shoot Se accumulation and less competitive inhibition by sulfate or by high‐S pretreatment. The selenate uptake rate for S. pinnata (1 h) was three‐ to four‐fold higher than for nonhyperaccumulators, and not significantly affected by 100‐fold excess sulfate, which reduced selenate uptake by 100% in S. elata and 40% in B. juncea . Real‐time reverse transcription PCR indicated constitutive upregulation in S. pinnata of sulfate transporters SULTR1;2 (root influx) and SULTR2;1 (translocation), but reduced SULTR1;1 expression (root influx). In S. pinnata , selenate uptake and translocation rates are constitutively elevated and relatively sulfate‐independent. Underlying mechanisms likely include overexpression of SULTR1;2 and SULTR2;1, which may additionally have evolved enhanced specificity for selenate over sulfate.