Transcription of the fbpl gene, encoding fructose-l,6-bisphosphatase, of Schizosaccharomyces pombe is subject to glucose repression. Previous work has demonstrated that several genes {g/t genes} are required for this repression. In this report we demonstrate that one of these genes, git2, is the same as the cyrl gene, which encodes adenylate cyclase, and that loss-of-function mutations in git2 cause constitutive fbpl transcription. Addition of cAMP to the growth medium suppresses the transcriptional defect in git2 mutants as well as in strains that carry mutations in any of six additional g/t genes. Similarly, exogenous cAMP represses [bpl transcription in wild-type cells grown on a derepressing carbon source. Different levels of adenylate cyclase activity in different git2 mutants, coupled with the result that some git2 mutants display intragenic complementation, strongly suggest that adenylate cyclase acts as a multimer and that different git2 mutations alter distinct activities of adenylate cyclase, including catalytic activity and response to glucose.Additional experiments demonstrate that this cAMP signaling pathway is independent of the S. pombe rasl gene and works by activation of cAMP-dependent protein kinase.