**1. Background**

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]. Furthermore, high levels of PA largely prevent the absorption of essential metals in the intestine, thus reducing further the nutritional value of the seeds [2,3].

In the last decades, several approaches have been proposed to solve the seed PA-related problems, including the engineering of crops for high phytase activity in seeds, or the selection of suitable *low phytic acid* (*lpa*) genotypes for crop breeding [4]. Today, numerous *lpa* genotypes have been identified and studied in several major crops, including maize, barley, wheat, rice, soybean, and common bean, reveling several mutations and alleles that could be potentially useful for breeding. However, a large part of the *lpa* phenotypes is caused by mutations in genes involved in PA biosynthesis or compartmentalization and often results in undesirable pleiotropic effects on yield-related traits and agronomic performances, since PA and inositol phosphates play pivotal roles in a plethora of developmental and signaling processes [4,5]. As a result, the use of these genetic resources to engineer seed PA content has proven to be challenging. Most recent advances in this research topic revealed that mutations in some members of the sulfate transporter gene family might result in *lpa* phenotypes. Unfortunately, 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.
