Plant architecture is an important agronomic trait and is useful for identification of plant species. The molecular basis of plant architecture, however, is largely unknown. Forward genetics was used to identify an Arabidopsis mutant with altered plant architecture. Using genetic and molecular approaches, we analyzed the roles of a mutated cyclophilin in the control of plant architecture. The Arabidopsis mutant roc1 has reduced stem elongation and increased shoot branching, and the mutant phenotypes are strongly affected by temperature and photoperiod. Map-based cloning and transgenic experiments demonstrated that the roc1 mutant phenotypes are caused by a gain-of-function mutation in a cyclophilin gene, ROC1. Besides, application of the plant hormone gibberellic acid (GA) further suppresses stem elongation in the mutant. GA treatment enhances the accumulation of mutated but not of wildtype (WT) ROC1 proteins. The roc1 mutation does not seem to interfere with GA biosynthesis or signaling. GA signaling, however, antagonizes the effect of the roc1 mutation on stem elongation. The altered plant architecture may result from the activation of an R gene by the roc1 protein. We also present a working model for the interaction between the roc1 mutation and GA signaling in regulating stem elongation.