Abstract
In higher plants, nearly all above ground organs are derived from the shoot apical meristem (SAM). We isolated the recessive Arabidopsis mutant gorgon (gor), which displays continuous enlargement of the SAM during postembryonic development. We mapped the gor mutation and identified a missense mutation in SHOOT MERISTEMLESS (STM), a homeobox gene required for SAM formation and maintenance. In contrast to gor, known loss-of-function mutants of STM display severe reduction of the SAM, suggesting that gor represents a novel STM allele whose effect on SAM development is opposite to that of the loss-of-function alleles. Transformation of a wild-type genomic fragment of STM into the gor background completely rescued the gor phenotype whereas the same fragment but with the gor mutation recapitulated the mutant phenotype when introduced into a loss-of-function allele of STM. These results demonstrate that the missense mutation in STM is responsible for the gor mutant phenotype. We analyzed the relationship between the gor and the other regulators of the SAM. Based on the results, the significance of the gor mutation on SAM development will be discussed
