Abstract

Phytic acid (myo‐inositol 1,2,3,4,5,6 hexakisphosphate) is the most abundant form of phosphorus (P) in seeds and is virtually indigestible by humans or non‐ruminant livestock. It was hypothesized that one class of maize (Zea mays L.) and barley (Hordeum vulgare L.) low phytic acid mutations, designated lpa1, interrupt myo‐inositol supply during seed development and may be mutations of the myo‐inositol 1‐phosphate synthase (MIPS) gene. This study describes the isolation, inheritance, and genetic mapping of the first rice lpa1 mutation and reexamines the MIPS/lpa1 candidate gene hypothesis in rice. Grain from 3632 rice M2 lines, derived from gamma‐irradiated seed, was screened for the lpa phenotype. Two mutations, one lethal and one non‐lethal, were identified. The non‐lethal mutation is phenotypically similar to maize and barley lpa1 mutants and was designated rice lpa1‐1 Homozygosity for rice lpa1‐1 reduces the phytic acid portion of seed P from 71 to 39% and increases the inorganic portion of seed P from 5 to 32%, with little effect on total seed P. This rice lpa1 mutation was mapped to a 2.2‐cM interval on chromosome 2L. A single‐copy rice MIPS gene was mapped to a locus on rice chromosome 3 that is orthologous to MIPS loci on maize chromosome 1S (near maize lpa1) and barley chromosome 4H. Unlike maize lpa1, the rice and barley lpa1 mutations loci are clearly distinguishable from this canonical MIPS gene. No relationship can be inferred between the maize, barley, and rice lpa1 loci. Although this canonical MIPS gene may be an appropriate target for controlling seed phytic acid synthesis, modifications of other genes (e.g., maize lpa2, barley lpa1, barley lpa2, and rice lpa1) may also be useful in reducing grain phytic acid and improving the nutritional value of cereal grains and/or milling by‐products.

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