Abstract

Carbohydrate partitioning from source to sink tissues is critical for plant growth and development. However, in maize (Zea mays L.), the molecular mechanisms of callose synthase gene regulating this process have seldom been reported. Here, we show that the mutation of maize callose synthase12 (ZmCals12) caused increased accumulation of carbohydrate in the photosynthetic leaves but reduced carbohydrate content in sink tissues, which led to plant dwarfing and male sterile. Histochemical GUS activity assay and mRNA in situ hybridization (ISH) indicated that ZmCals12 was mainly expressed in the vascular transport system. Loss-of-function of ZmCals12 reduced callose synthase activity and callose deposition in plasmodesmatas (PDs) and around phloem cells (PCs) of vascular bundle. The drop-and-see (DANS) assay revealed that the PD permeability in the photosynthetic cells and the transport competence of leaf veins were reduced in the Zmcals12 mutants, which led to the reduced symplastic transport. Paraffin section experiment revealed that less-developed vascular cells (VCs) in the Zmcals12 mutants potentially disturbed sugar transport, thus resulting in the pleiotropic phenotype of the Zmcals12 mutants. In addition, the impaired sugar transport hindered the internode development by inhibiting auxin (IAA) biosynthesis and signaling in the Zmcals12 mutant. Collectively, our results provide insights into the mechanism of ZmCals12-mediated callose deposition and symplastic transport governing maize growth and development.

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