Abstract
Background: As the main form of photoassimilates transported from vegetative tissues to the reproductive organs, sucrose and its degradation products are crucial for cell fate determination and development of maize kernels. Despite the relevance of sucrose synthase SH1 (shrunken 1)-mediated release of hexoses for kernel development, the underlying physiological and molecular mechanisms are not yet well understood in maize (Zea mays). Results: Here, we identified a new allelic mutant of SH1 generated by EMS mutagenesis, designated as sh1*. The mutation of SH1 caused more than 90% loss of sucrose synthase activity in sh1* endosperm, which resulted in a significant reduction in starch contents while a dramatic increase in soluble sugars. As a result, an extremely high osmolality in endosperm cells of sh1* was generated, which caused kernel swelling and affected the seed development. Quantitative measurement of phosphorylated sugars showed that Glc-1-P in endosperm of sh1* (17 μg g- 1 FW) was only 5.2% of that of wild-type (326 μg g- 1 FW). As a direct source of starch synthesis, the decrease of Glc-1-P may cause a significant reduction in carbohydrates that flow to starch synthesis, ultimately contributing to the defects in starch granule development and reduction of starch content. Conclusions: Our results demonstrated that SH1-mediated sucrose degradation is critical for maize kernel development and starch synthesis by regulating the flow of carbohydrates and maintaining the balance of osmotic potential.