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pubmed:abstractText |
Wild-type stomata are distributed nonrandomly, and their density is controlled by endogenous and exogenous factors. In the Arabidopsis mutant stomatal density and distribution1-1 (sdd1-1), the establishment of the stomatal pattern is disrupted, resulting in stomata clustering and twofold to fourfold increases in stomatal density. The SDD1 gene that encodes a subtilisin-like Ser protease is expressed strongly in stomatal precursor cells (meristemoids and guard mother cells), and the SDD1 promoter is controlled negatively by a feedback mechanism. The encoded protein is exported to the apoplast and probably is associated with the plasma membrane. SDD1 overexpression in the wild type leads to a phenotype opposite to that caused by the sdd1-1 mutation, with a twofold to threefold decrease in stomatal density and the formation of arrested stomata. While SDD1 overexpression was effective in the flp mutant, the tmm mutation acted epistatically. Thus, we propose that SDD1 generates an extracellular signal by meristemoids/guard mother cells and demonstrate that the function of SDD1 is dependent on TMM activity.
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