The <i>SHOOT MERISTEMLESS</i> gene is required for maintenance of undifferentiated cells in <i>Arabidopsis</i> shoot and floral meristems and acts at a different regulatory level than the meristem genes <i>WUSCHEL</i> and <i>ZWILLE</i>

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<jats:title>Summary</jats:title><jats:p>The function of the <jats:italic>SHOOT MERISTEMLESS (STM)</jats:italic> gene in shoot and floral meristems throughout <jats:italic>Arabidopsis</jats:italic> development has been analyzed. The results show that <jats:italic>STM</jats:italic> plays a major role in maintaining shoot and floral meristems. In an allelic series of <jats:italic>stm</jats:italic> mutants the shoot meristem was either reduced or completely absent in mature embryos and mutant seedling cotyledons showed partial fusion, indicating that the <jats:italic>STM</jats:italic> gene affects embryonic shoot meristem development and spacing of cotyledons. Postembryonically, <jats:italic>stm</jats:italic> mutants initiated adventitious shoot development at a position corresponding to the shoot meristem in wild‐type. Repetitively initiated defective mutant shoot and floral meristems were consumed during primordia formation and typically terminated prematurely in fused ectopic primordia, indicating that <jats:italic>STM</jats:italic> is required for continuous shoot and floral meristem function.</jats:p><jats:p>Analogous defects were observed in <jats:italic>stm</jats:italic> embryonic and postembryonic development suggesting that similar mechanisms are employed in embryonic and postembryonic organ primordia initiation. Allelic combinations suggest different thresholds for <jats:italic>STM</jats:italic> requirement during plant development. <jats:italic>STM</jats:italic> requirement could not be bypassed by standard growth factor regimes or by shoot regeneration from calli. The results suggest that <jats:italic>STM</jats:italic> functions by preventing incorporation of cells in the meristem center into differentiating organ primordia and that this role can completely account for all defects observed in <jats:italic>stm</jats:italic> mutants.</jats:p><jats:p>Mutations in the <jats:italic>WUSCHEL (WUS)</jats:italic> and <jats:italic>ZWILLE (ZLL)</jats:italic> genes result in defective organization and premature termination of shoot meristems. Genetic interactions between <jats:italic>STM, WUS</jats:italic> and <jats:italic>ZLL</jats:italic> were analyzed and the results indicate that <jats:italic>STM</jats:italic> acts upstream of <jats:italic>WUS</jats:italic> and <jats:italic>ZLL</jats:italic>. Therefore, while <jats:italic>STM</jats:italic> appears to function in keeping central meristem cells undifferentiated, <jats:italic>WUS</jats:italic> and <jats:italic>ZLL</jats:italic> seem to be subsequently required for proper function of these cells.</jats:p>

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