**7. Concluding Remarks**

Ultimately, understanding the genetic mechanisms for controlling PP-InsP synthesis and function is critical for developing novel low-phytate crops that are not compromised by changes in PP-InsP signaling. A recent review nicely details existing transgenic strategies used to reduce phytate in plants [76]. A common strategy is to use tissue-specific promoters to drive the overexpression of enzymes that break down InsP6, such as Phytase, or to knock-down the expression of genes required for InsP6 synthesis. By doing so, the idea is that only specific tissues will have reduced InsP6. This strategy works well to reduce InsP6 in seeds, for example, without negatively impacting vegetative tissues. One potential drawback of this approach is that the reduction in InsP6 may also a ffect the precursor available for PP-InsP synthesis in these transgenic plants. It is also important to consider that plants store approximately 1% InsP7 and InsP8 in seeds [5]. We do not know much currently about whether and how PP-InsPs might regulate seed phosphate storage, however, we point out that existing data on *mrp5* InsP6 transporter mutants indicate that InsP6 modulation in seed can result in increases in PP-InsPs [5]. Given the emerging role of PP-InsPs in controlling critical plant sensing and signaling pathways, the future development of strategies for phytate reduction without compromising PP-InsP synthesis and function should be considered by plant breeders.

**Author Contributions:** Conceptualization, C.F., G.G. and O.A.; writing—original draft preparation, C.F., G.G. and O.A.; writing—review and editing, C.F. All authors have read and agreed to the published version of the manuscript.

**Funding:** We gratefully acknowledge the NSF for funding to GG (MCB 1616038). This work is supported in part by the USDA National Institute of Food and Agriculture, Hatch project VA-136334.

**Conflicts of Interest:** The authors declare no conflict of interest.
