The timing of the transitions between the juvenile and adult vegetative stages (vegetative phase change) is important for shoot maturation in plants. The juvenile and adult vegetative stages are defined by a difference in reproductive competence (incompetent versus competent), but they are also associated with a variety of other morphological and physiological differences. An evolutionarily conserved microRNA, miR156, plays a central role in promoting the juvenile phase through its repression of ten adult-phase-inducing SPL family transcription factors. A decrease in miRI56 abundance and a concomitant increase in SPL expression are correlated with the onset of adult traits. However, despite the importance of miR156 in regulating vegetative phase change, very little is known about the regulation of miR156 itself at either transcriptional or posttranscriptional levels. The aim of this work is to further the understanding of the factors that contribute to the regulation of miR156.

To identify the source of signals that repress miR156 and promote vegetative phase change, I performed organ ablation experiments in Arabidopsis. I discovered that defoliation, but not root or cotyledon ablation, delayed phase change, and this effect was attributable to an increase in the expression of MIR156. Defoliation also delayed phase change in Nicotiana benthamiana, Zea mays (maize), and Acacia mangium. Based on these results, I concluded that vegetative phase change is mediated by a leaf-derived signal that represses the transcription of MIR156. Furthermore, the possibility that sugar is the leaf signal was explored. Exogenous sugar repressed the expression of MIR156, resulting in an increase in SPL expression and early phase change. Consistent with this observation, mutants with reduced abundance of endogenous sugars had elevated miR156 expression and delayed phase change. This sugar response was dependent on the signaling function of the glucose sensor HXK1. To identify additional modifiers of the miR156 pathway, I performed a genetic screen using an SPL3-GFP translational reporter, identifying mutants that have either higher or lower GFP expression. This screen produced mutations in SUO, a BAH domain containing protein. SUO is a Processing-body (P-body) component and is specifically required for miR156-mediated translational repression, but not for miR156-mediated transcript cleavage. These results indicate that miR156-mediated translational repression plays an important role in regulating vegetative phase change.