Abstract
Plants are able to reiteratively form new organs in an environmentally adaptive manner during postembryonic development. Organ formation in plants is dependent on stem cell niches (SCNs), which are located in the so-called meristems. Meristems show a functional zonation along the apical-basal axis and the radial axis. Shoot apical meristems of higher plants are dome-like structures, which contain a central SCN that consists of an apical stem cell pool and an underlying organizing center. Organ primordia are formed in the circular peripheral zone (PZ) from stem cell descendants in which differentiation programs are activated. One mechanism to keep this radial symmetry integrated is that the existing SCN actively suppresses stem cell identity in the PZ. However, how this lateral inhibition system works at the molecular level is far from understood. Here, we show that a defect in the putative carboxypeptidase ALTERED MERISTEM PROGRAM1 (AMP1) causes the formation of extra SCNs in the presence of an intact primary shoot apical meristem, which at least partially contributes to the enhanced shoot meristem size and leaf initiation rate found in the mutant. This defect appears to be neither a specific consequence of the altered cytokinin levels in amp1 nor directly mediated by the WUSCHEL/CLAVATA feedback loop. De novo formation of supernumerary stem cell pools was further enhanced in plants mutated in both AMP1 and its paralog LIKE AMP1, indicating that they exhibit partially overlapping roles to suppress SCN respecification in the PZ.
Highlights
Plants are able to reiteratively form new organs in an environmentally adaptive manner during postembryonic development
The amp1-1 shoot meristematic area was approximately three times bigger compared with the wild type (Fig. 1E), and it exhibited a broader and higher meristem dome (Fig. 1B)
To analyze whether increased meristem size correlated with altered organizing center (OC) organization, we performed WUS:: GUS reporter analysis in amp1-1 median longitudinal shoot apical meristem (SAM) sections
Summary
Max-Planck-Institut für Molekulare Pflanzenphysiologie, Am Mühlenberg 1, D–14476 Potsdam-Golm, Germany. How SAM architecture and activity is altered in detail in amp and to which extent these SAM-related defects can be directly attributed to the elevated CK biosynthesis rate found in the mutant are important unsolved questions to better position AMP1 function in the known regulatory network controlling SAM development. To this end, we dissected the causal relationship of amp phenotypes and altered CK accumulation and found that SAM size and SAM primordia. We show that LIKE AMP1 (LAMP1) acts partially redundantly with AMP1 to suppress OC respecification in the PZ in the presence of an intact SCN
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