The Arabidopsis GAI gene defines a signaling pathway that negatively regulates gibberellin (GA) responses. The gai mutant allele of Arabidopsis shows reduced GA responsiveness. Researchers cloned the GAI gene and found that it is closely related to GRS. The GAI and GRS proteins contain nuclear localization signals, a region homologous to a putative transcription factor, and motifs characteristic of transcriptional coactivators. Genetic analysis indicates that GAI is a repressor of GA responses, and GA can release this repression. The gai mutant is resistant to GA effects, suggesting it is a mutant repressor. Mutations at SPY and GAR2 suppress the gai phenotype, indicating that GAI, SPY, and GAR2 are involved in a signaling pathway that negatively regulates GA responses. This pathway suggests that GA modulates plant growth through derepression rather than simple stimulation. The GAI gene is closely related to the predicted product of the Arabidopsis gene SCARECROW (SCR), a member of a novel family of candidate transcription factors. GAI contains a consensus nuclear localization signal, a LXXLL motif, and is a new member of the VHIID domain family. GAI null alleles confer increased resistance to the growth-retarding effects of PAC, an inhibitor of GA biosynthesis. These observations suggest that GAI is a negative regulator of GA responses, and that its loss of function reduces GA dependency in growth. The gai mutant allele encodes an altered product, and the gai-t6 allele contains a transposed Ds that interrupts a transcribed gene. The gai-t6 allele is a likely null allele and confers increased PAC resistance. The gai-suppressor mutations spy-7 and gar2-1 cause partial suppression of the gai phenotype and also suppress the effect of gai on the accumulation of C-20 oxidase transcripts. These mutations act as GA signal transduction components upstream or downstream of the GAI gene product. The additive effects of spy-7 and gar2-1 suggest they identify different branches of the GA signaling pathway. The GAI gene is a repressor of stem elongation, and GA derepresses stem elongation by opposing GAI action. The segment missing in the mutant gai protein could be responsible for interacting with the GA signal or GA itself. The gai mutant protein is relatively resistant to GA and represses growth in a dominant fashion. Null alleles at GAI confer a tall, PAC-resistant phenotype because the absence of GAI results in loss of its growth repression function. The gai-t6 mutant is not totally PAC resistant because of the probable activity of GRS. The GA signaling system outlined in this paper has several intriguing properties. It is no longer essential if the GA signaling system is compromised. The different degrees of PAC resistance exhibited by the various mutants show that the GA signaling system is capable of eliciting a graduated, rather than anThe Arabidopsis GAI gene defines a signaling pathway that negatively regulates gibberellin (GA) responses. The gai mutant allele of Arabidopsis shows reduced GA responsiveness. Researchers cloned the GAI gene and found that it is closely related to GRS. The GAI and GRS proteins contain nuclear localization signals, a region homologous to a putative transcription factor, and motifs characteristic of transcriptional coactivators. Genetic analysis indicates that GAI is a repressor of GA responses, and GA can release this repression. The gai mutant is resistant to GA effects, suggesting it is a mutant repressor. Mutations at SPY and GAR2 suppress the gai phenotype, indicating that GAI, SPY, and GAR2 are involved in a signaling pathway that negatively regulates GA responses. This pathway suggests that GA modulates plant growth through derepression rather than simple stimulation. The GAI gene is closely related to the predicted product of the Arabidopsis gene SCARECROW (SCR), a member of a novel family of candidate transcription factors. GAI contains a consensus nuclear localization signal, a LXXLL motif, and is a new member of the VHIID domain family. GAI null alleles confer increased resistance to the growth-retarding effects of PAC, an inhibitor of GA biosynthesis. These observations suggest that GAI is a negative regulator of GA responses, and that its loss of function reduces GA dependency in growth. The gai mutant allele encodes an altered product, and the gai-t6 allele contains a transposed Ds that interrupts a transcribed gene. The gai-t6 allele is a likely null allele and confers increased PAC resistance. The gai-suppressor mutations spy-7 and gar2-1 cause partial suppression of the gai phenotype and also suppress the effect of gai on the accumulation of C-20 oxidase transcripts. These mutations act as GA signal transduction components upstream or downstream of the GAI gene product. The additive effects of spy-7 and gar2-1 suggest they identify different branches of the GA signaling pathway. The GAI gene is a repressor of stem elongation, and GA derepresses stem elongation by opposing GAI action. The segment missing in the mutant gai protein could be responsible for interacting with the GA signal or GA itself. The gai mutant protein is relatively resistant to GA and represses growth in a dominant fashion. Null alleles at GAI confer a tall, PAC-resistant phenotype because the absence of GAI results in loss of its growth repression function. The gai-t6 mutant is not totally PAC resistant because of the probable activity of GRS. The GA signaling system outlined in this paper has several intriguing properties. It is no longer essential if the GA signaling system is compromised. The different degrees of PAC resistance exhibited by the various mutants show that the GA signaling system is capable of eliciting a graduated, rather than an