Abstract
Plants show an indeterminate mode of growth by the activity of organ forming stem cell niches in apically positioned meristems. The correct formation and activity of these meristems are a prerequisite for their adaptive development and also allow the maintenance of organogenesis under adverse circumstances such as wounding. Mutation of the putative Arabidopsis (Arabidopsis thaliana) Glu carboxypeptidase ALTERED MERISTEM PROGRAM1 (AMP1) results in Arabidopsis plants with enlarged shoot apical meristems, supernumerary stem cell pools, and higher leaf formation rate. AMP1 deficiency also causes exaggerated de novo formation of shoot meristems. The activity of AMP1 has been implicated in the control of microRNA (miRNA)-dependent translation; however, it is not known how this function contributes to the shoot meristem defects. Here, we show that the transcription factor RAP2.6L is upregulated in the Arabidopsis amp1 mutant. Overexpression of RAP2.6L in the wild type causes amp1 mutant-related phenotypic and molecular defects, including enhanced shoot regeneration in tissue culture. Conversely, inhibition of RAP2.6L in the amp1 mutant suppresses stem cell hypertrophy and the regenerative capacity. We further provide evidence that RAP2.6L is under direct transcriptional control of miRNA-regulated class III homeodomain-Leu zipper (HD-ZIP III) proteins, key regulators of shoot meristem development, which overaccumulate in the amp1 mutant. Our results reveal a transcription factor module acting downstream of AMP1 in the control of shoot stem cell niche patterning. By positioning the HD-ZIP III/RAP2.6L module downstream of AMP1 function, we provide a mechanistic link between the role of AMP1 in miRNA-mediated translational repression and shoot stem cell specification.