Phenotype suppression: a postulated molecular mechanism for mediating the relationship of proliferation and differentiation by Fos/Jun interactions at AP-1 sites in steroid responsive promoter elements of tissue-specific genes
Department of Cell Biology
Animals; Base Sequence; *Cell Differentiation; *Cell Division; DNA-Binding Proteins; Humans; Molecular Sequence Data; Osteoblasts; Osteocalcin; Phenotype; *Promoter Regions, Genetic; Protein-Tyrosine Kinases; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-fos; Proto-Oncogene Proteins c-jun; *Suppression, Genetic; Transcription Factors; Transcription, Genetic; Vitamin D
There is a generalized reciprocal relationship between cell growth and expression of genes that occurs following completion of proliferation, which supports the progressive development of cell and tissue phenotypes. Molecular mechanisms which couple the shutdown of proliferation with initiation of tissue-specific gene transcription have been addressed experimentally in cultures of primary diploid osteoblasts that undergo a growth and differentiation developmental sequence. Evidence is presented for a model which postulates that genes transcribed post-proliferatively are suppressed during cell growth by binding of the Fos/Jun protein complex to AP-1 promoter sites associated with vitamin D responsive elements of several genes encoding osteoblast phenotype markers (Type I collagen, alkaline phosphatase, osteocalcin).
DOI of Published Version
J Cell Biochem. 1991 Jan;45(1):9-14. Link to article on publisher's site
Journal of cellular biochemistry
Lian JB, Stein GS, Bortell R, Owen TA. (1991). Phenotype suppression: a postulated molecular mechanism for mediating the relationship of proliferation and differentiation by Fos/Jun interactions at AP-1 sites in steroid responsive promoter elements of tissue-specific genes. Stein, Stein, Lian, vanWijnen Lab Publications. https://doi.org/10.1002/jcb.240450106. Retrieved from https://escholarship.umassmed.edu/stein/118