(1) A functional analysis of deletions in the promoter of the mouse Alpha2(I) collagen gene indicates there are two different segments far upstream of the start of transcription that are important for optimal expression of this gene. (2) Transgenic mice were generated in which an alpha2(I) collagen promoter-chloramphenicol acetylase chimeric gene has been stably introduced in the germline. These new mouse strains show a tissue specific pattern of expression for the chimeric gene that coincides with that of the endogenous type I collagen genes. (3) Mutant NIH 3T3 fibroblasts have been obtained in which type I collagen and fibronectin genes escape from the transcriptional control which normally inhibits their in v-mos transformed cells. (4) A segment with dyad symmetry around the translation initiation site of alpha2(I) collagen mRNA exerts a strong inhibition on the level of translation of this mRNA. (5) The presence of v-fos in NIH 3T3 cells strongly stimulates expression of the alpha1(III) collagen gene. This stimulation is mediated by transcriptional activation of the promoter for this gene.