The floral homeotic gene APETALA3 (AP3) is required for stamen and petal development in Arabidopsis. The previously described ap3-1 allele is temperature sensitive and carries a missense mutation near a 5' splice site. The missense mutation lies within a domain of the AP3 protein that is thought to be important for protein-protein interactions, which suggests that temperature sensitivity of ap3-1 could reflect an unstable interaction with cofactors. Here, we show instead that the ap3-1 mutation causes a temperature-dependent splicing defect and that temperature sensitivity is not a property of the protein products of ap3-1 but of RNA processing, possibly because of unstable base pairing between the transcript and small nuclear RNAs. The unexpected defect of the ap3-1 mutant offers unique opportunities for genetic and molecular studies of splice site recognition in plants.