In a previous work, it was shown that bicarbonate (one of the most important factors causing Fe chlorosis in Strategy I plants) can limit the expression of several genes involved in Fe acquisition. Hypoxia is considered another important factor causing Fe chlorosis, mainly on calcareous soils. However, to date it is not known whether hypoxia aggravates Fe chlorosis by affecting bicarbonate concentration or by specific negative effects on Fe acquisition.
View Article and Find Full Text PDFThe FeEDDHA [iron(3+) ethylenediamine di(o-hydroxyphenylacetic) acid] is one of the most efficient iron chelates employed in the correction of iron clorosis in calcareous soils. FeEDDHA presents different positional isomers: the ortho-ortho (o,o), the ortho-para (o,p), and the para-para (p,p). Of these isomers, the p,p cannot chelate Fe in soil solution in a wide range of pH values, while both o,o and o,p can.
View Article and Find Full Text PDFBicarbonate is considered one of the most important factors causing Fe chlorosis in Strategy I plants, mainly on calcareous soils. Most of its negative effects have been attributed to its capacity to buffer a high pH in soils, which can diminish both Fe solubility and root ferric reductase activity. Besides its pH-mediated effects, previous work has shown that bicarbonate can inhibit the induction of enhanced ferric reductase activity in Fe-deficient Strategy I plants.
View Article and Find Full Text PDFIn previous works using ethylene inhibitors and precursors, it has been shown that ethylene participates in the regulation of several Fe deficiency stress responses by Strategy I plants, such as enhanced ferric reductase activity, rhizosphere acidification and subapical root hair development. Furthermore, recent evidence suggests that ethylene could regulate the expression of both the ferric reductase and the iron transporter genes of Strategy I plants by affecting the FER (or FER-like) transcription factor. Recently, two H(+)-ATPase genes have been isolated from cucumber roots, CsHA1 and CsHA2.
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