Abstract
A few new papers report that mutations in some genes belonging to the group 3 of plant sulfate transporter family result in low phytic acid phenotypes, drawing novel strategies and approaches for engineering the low-phytate trait in cereal grains. Here, we shortly review the current knowledge on phosphorus/sulfur interplay and sulfate transport regulation in plants, to critically discuss some hypotheses that could help in unveiling the physiological links between sulfate transport and phosphorus accumulation in seeds.
Highlights
Phytic acid (PA)—the major phosphorus (P) store in seeds—cannot be digested by humans and monogastric animals who lack the digestive enzyme phytase
Most recent advances in this research topic revealed that mutations in some members of the sulfate transporter gene family might result in lpa phenotypes
Little data are available to explain such effects fully or to develop new strategies for engineering seed PA content. Trying to fill this gap, here, we shortly review the current knowledge on plant sulfate transporters, trying to provide a glimpse into the complex and, in many respects, unexpected connections among the regulatory layers of sulfur (S) and P homeostasis in plants
Summary
Phytic acid (PA)—the major phosphorus (P) store in seeds—cannot be digested by humans and monogastric animals who lack the digestive enzyme phytase. For this reason, almost 90% of phytate consumed by humans is excreted, contributing to eutrophication of rivers, lakes, and oceans [1]. Little data are available to explain such effects fully or to develop new strategies for engineering seed PA content. Trying to fill this gap, here, we shortly review the current knowledge on plant sulfate transporters, trying to provide a glimpse into the complex and, in many respects, unexpected connections among the regulatory layers of sulfur (S) and P homeostasis in plants
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