ArticleProceedings of the National Academy of Sciences of the United States of America1997
Chondrocytes as a specific target of ectopic Fos expression in early development.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 33 citations in OpenAlex.
- Combined Transcriptomics and Metabolomics Identify Regulatory Mechanisms of Porcine Vertebral Chondrocyte Development In Vitro.International journal of molecular sciences · 2024Article
- Article
- c-Fos induces chondrogenic tumor formation in immortalized human mesenchymal progenitor cells.Scientific reports · 2018Article
- Review
- Retinoic acid and the transcription factor MafB act together and differentially to regulate aggrecan and matrix metalloproteinase gene expression in neonatal chondrocytes.Journal of cellular biochemistry · 2013Article
- Article
- A cis-regulatory site downregulates PTHLH in translocation t(8;12)(q13;p11.2) and leads to Brachydactyly Type E.Human molecular genetics · 2010Article
- Molecular basis for skeletal variation: insights from developmental genetic studies in mice.Birth defects research. Part B, Developmental and reproductive toxicology · 2007Review
- Kinetics of v-src-induced epithelial-mesenchymal transition in developing glandular stomach.Oncogene · 2003Article
- Transcription factor ERG variants and functional diversification of chondrocytes during limb long bone development.The Journal of cell biology · 2000Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Finkel-Biskis-Jinkins murine sarcoma virus, which carries v-fos, induces osteosarcomas, whereas high-level expression of exogenous c-fos in transgenic and chimeric mice leads to postnatal development of osteogenic and chondrogenic tumors, respectively. To test whether such target cell specificity of an oncogene can be detected even in early development, we induced ectopic expression of fos in chicken limb buds by microinjecting replication-competent retrovirus into the presumptive leg field of stage 10 embryos. This caused cartilage truncation of all the long bones of the injected leg, which was mainly attributable to chondrodysplasia due to severe retardation of differentiation of the proliferating chondrocytes into mature or hypertrophic chondrocytes, as well as a slight delay in precartilagenous condensation. Expression of genes for all the other known members of chicken AP-1, which include such transforming genes as c-jun and fra-2, however, caused no macroscopic abnormalities in limb formation, indicating a specific function of Fos proteins in embryonic endochondral bone differentiation. The extent of truncation was stronger with v-Fos than with c-Fos, and comparative analysis of these proteins, as well as v-Fos mutants, revealed that strong transforming activity of Fos protein is necessary to cause dysplasia, suggesting that common molecular mechanisms are involved in both embryonic chondrodysplasia and bone tumor formation in postnatal mice.
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