Abstract

The opaque-2 (o2) mutation of maize increases lysine content, but the low seed density and soft texture of this type of mutant are undesirable. Lines with modifiers of the soft kernel phenotype (mo2) called “Quality Protein Maize” (QPM) have high lysine and kernel phenotypes similar to normal maize. Prior research indicated that the formation of vitreous endosperm in QPM might involve changes in starch granule structure. In this study, we focused on analysis of two starch biosynthetic enzymes that may influence kernel vitreousness. Analysis of recombinant inbred lines derived from a cross of W64Ao2 and K0326Y revealed that pullulanase activity had significant positive correlation with kernel vitreousness. We also found that decreased Starch Synthase III abundance may decrease the pullulanase activity and average glucan chain length given the same Zpu1 genotype. Therefore, Starch Synthase III could indirectly influence the kernel vitreousness by affecting pullulanase activity and coordinating with pullulanase to alter the glucan chain length distribution of amylopectin, resulting in different starch structural properties. The glucan chain length distribution had strong positive correlation with the polydispersity index of glucan chains, which was positively associated with the kernel vitreousness based on nonlinear regression analysis. Therefore, we propose that pullulanase and Starch Synthase III are two important factors responsible for the formation of the vitreous phenotype of QPM endosperms.

Highlights

  • Normal maize lines cannot provide a nutritionally balanced source of protein because of the deficiency of lysine [1]

  • Previous sequence analysis of starch biosynthesis genes showed that synthase IIa (SSIIa), synthase IIb (SSIIb), synthase III (SSIII) and Zpu1 were hypothesized to be the candidate genes that influence the kernel phenotypes of Quality Protein Maize (QPM) lines

  • Some evidence showed that the QPM amylopectin branching pattern was most similar to the SSII mutant in maize and rice [25], and the SSIIa mutation increased the proportion of short amylopectin branches [25, 33]

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Summary

Introduction

Normal maize lines cannot provide a nutritionally balanced source of protein because of the deficiency of lysine [1]. The opaque (o2) mutation of maize markedly changes the amino acid balance, and results in a substantial increase in the lysine content [3]. Previous studies discovered that the starchy (or opaque) phenotype is associated with reduced protein body size and lower amounts of 22-kD α-zein, a prolamin storage protein in the endosperm [5, 6]. The cellular and biochemical mechanisms that cause the opaque phenotype are not well understood but recent evidence indicates that an important factor is the ratio and arrangement of zein protein isoforms within the substructure of protein bodies [9, 10]

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