ALTERED MERISTEM PROGRAM1Suppresses Ectopic Stem Cell Niche Formation in the Shoot Apical Meristem in a Largely Cytokinin-Independent Manner  

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.

The small molecule hyperphyllin enhances leaf formation rate and mimics shoot meristem integrity defects associated with AMP1 deficiency

“…4B). Moreover, the previously reported amp1-specific formation of ectopic OCs in the SAM periphery (Huang et al, 2015) was phenocopied in wild type by HP treatment (Fig. 4,C and D).…”

“…During the vegetative growth phase the enlarged mutant shoot apex generates leaves at a much higher pace and with altered phyllotaxis (Chaudhury et al, 1993;Nogué et al, 2000a). Moreover, vegetative SAM enlargement and increased organ formation rate correlate and might be at least partially driven by a strong tendency to generate ectopic stem cell niches in the SAM periphery (Huang et al, 2015). Similar SAM-related phenotypes were also observed in mutants of AMP1 orthologs of corn (Zea mays), rice (Oryza sativa), and Lotus japonicus, suggesting that its role in shoot development is conserved among flowering plants (Suzuki et al, 2008;Kawakatsu et al, 2009;Suzaki et al, 2013).…”

“…4A). Another marker with an altered expression pattern in amp1 is the organizing center (OC) defining transcription factor WUSCHEL (WUS; Huang et al, 2015). The zone of WUS::GUS activity was substantially broadened in both amp1-1 and in drug-treated wildtype SAMs compared to the mock-treated wild-type control (Fig.…”

“…However, to explain the range of phenotypes by a defect in one of the classical hormone pathways turned out to be difficult. Cytokinin (CK) biosynthesis has been shown to be up-regulated in amp1 (Chin-Atkins et al, 1996;Nogué et al, 2000b;Saibo et al, 2007;Huang et al, 2015). Whereas the increased CK levels appear to be responsible for de-etiolation in the dark, increased shoot branching, and enhanced tolerance against nitric oxide , it has been recently shown that they are a consequence rather than a cause of the abnormal SAM phenotypes found in the mutant (Huang et al, 2015).…”

“…Cytokinin (CK) biosynthesis has been shown to be up-regulated in amp1 (Chin-Atkins et al, 1996;Nogué et al, 2000b;Saibo et al, 2007;Huang et al, 2015). Whereas the increased CK levels appear to be responsible for de-etiolation in the dark, increased shoot branching, and enhanced tolerance against nitric oxide , it has been recently shown that they are a consequence rather than a cause of the abnormal SAM phenotypes found in the mutant (Huang et al, 2015). Depending on the subset of phenotypes analyzed, several studies also reported alterations in other hormonal pathways including ethylene, gibberellin, abscisic acid, and auxin (Saibo et al, 2007;Vidaurre et al, 2007;Griffiths et al, 2011;Shi H et al, 2013;Yao et al, 2014).…”