Barton 9724163 The shoot apical meristem (SAM) plays a central role in angiosperm shoot development giving rise to nearly all of the above-ground structures of the plant. The SAM simultaneously serves two purposes: it acts both as a site of pattern formation and as a source of pluripotent stem cells or initial cells. Thus, the SAM produces the basic subunits of the shoot, leaves and stem, in repeated and predictable patterns, using new cells derived from the center of the SAM. The long term goal of this project is to understand the molecular basis for how a SAM makes a plant. By isolating mutants that either entirely lack a SAM or are defective in some aspect of SAM development, it is possible to identify genes that are uniquely important in SAM function. One of these is the SHOOTMERISTEMLESS (STM) gene, a homeodomain-containing gene that is required for SAM formation and function in the model plant Arabidopsis. The STM appears to act in the periphery of the SAM to form the separations between organs, and in doing so, may play an important role in the shaping of the plant body. We will test this notion by specifically expressing the STM gene product in the periphery of the SAM and asking whether this can rescue the defect in cotyledon separation in stm mutants. This experiment will also allow us to gauge the degree to which STM acts cell autonomously within the SAM. Other mutants defective in SAM development will be studied as well. A Peripheral Zone specific reporter construct will be used to determine if several mutants suggested to have defects in the Central Zone misexpress this construct. The PINHEAD gene, a gene required for the correct functioning of positional information in the SAM, will be cloned to find out how positional information works in the SAM - a process about which almost nothing is known. Finally, the Adnormal mutant has suggested the existence of a positive interaction between the adaxial side of the leaf and SAM formation. We will test this hypothesis by i solating mutants that do not make an adaxial leaf domain and asking whether they can form axillary and primary SAMs. We will also investigate the ability of an "overly" adaxialized mutant to suppress the phenotypes of mutants defective in SAM formation.
