Toward molecular understanding of flower senescence/abscission, we have identified a mutant, designated as dea1-1D (dealyed abscission1-1D), with delayed flower senescence/abscission syndrome from activation-tagged pools. Phenotypic analysis revealed pleiotropic effects of dea1-1D mutation including delayed flowering as well as smaller serrated leaves. Genetic analysis showed that it is a dominant mutation. Molecular analysis on the flower senescence syndrome indicated that dea1-1D might define novel regulatory branch of flower abscission, controlling expression of ethylene-responsive AP2 transcription factor. On the contrary, triple responses was not affected by dea1-1D mutant. Though the penetrance was not complete, the mutant phenoytpes was shown to be tightly linked with the T-DNA selection marker, BASTA-resistance. We identified the T-DNA insertion site through molecular cloning of the T-DNA flanking genomic DNA and found that a neighboring gene was overexpressed in the dea1-1D mutant. Together with gene expression analysis, we will discuss possible function of DEA1 during flower senescence and abscission.