C1 is a regulatory locus of the anthocyanin pathway in Zea mays L. The locus is specifically expressed in the aleurone and scutellum tissue of maize kernels. The C1 protein sequence has homology to myb proto-oncogene products and the protein might act as a transcriptional activator;The research presented here involves the analysis of two recessive C1 alleles: c1-p and c1-m1. In homozygous c1-p maturing kernels there is no anthocyanin production, but those kernels produce anthocyanin when germinated in the presence of light. The DNA sequence analysis of the c1-p genomic clone is presented. The sequence revealed minor alterations in the promoter and that the predicted coding region is essentially unaltered. Several major deletions in the 3[superscript]' region of the c1-p allele were also detected. One of the deletions removed the standard poly(A) addition site. A second deletion included the area where the defective transposable element Ds is inserted in the mutant c1-m1;The c1-m1 allele arose from the transposition of the "standard" Ds, which causes chromosome breakage, from its original position into the C1 locus. When this Ds element excises, gene function can be restored or chromosome breaks can occur. The preliminary sequence analysis of c1-m1 is presented. The sequence revealed several interesting features: (1) The Ds element is inserted 2 kb downstream of the translation stop codon. (2) Except for the Ds insertion, there seems to be only minor base pair alterations in the C1 specific sequence. (3) The Ds element is an Ac deletion derivative and not a Double Ds. It was previously postulated that Double Ds elements are responsible for chromosome breakage, but the sequence data of c1-m1 indicates that other Ds elements can cause breaks;The combined analysis of c1-p and c1-m1 indicated that the 3[superscript]' region of the C1 gene, specifically where Ds is inserted in the mutant c1-m1, is important for normal expression. Several hypotheses are presented to provide a model for further research to determine why the alterations in these alleles resulted in their mutant phenotype.