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